Overview and details of the sessions of this conference. Please select a date or location to show only sessions at that day or location. Please select a single session for detailed view (with abstracts and downloads if available).
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Session Overview |
Date: Tuesday, 13/June/2023 | ||
8:00am - 6:30pm |
Slides Center Location: Slides Center |
Registration Desk Location: Bologna Congress Center |
9:00am - 10:45am |
Session 3.1: Inflammation and Immunity as mitochondrial contributor to pathology Location: Bologna Congress Center - Sala Europa Chair: Jose Antonio Enriquez Chair: Daria Diodato Invited Speakers:
S. Pluchino; M. Mittelbrunn
Fuels and drivers of smouldering brain disease University of Cambridge, United Kingdom Invited Immunometabolisms at the crossroad between inflammation and aging CSIC- Consejo Superior de Investigaciones Cientificas, Spain Oral presentation Dissecting the role of type I interferon signaling in microglial response in a mouse model of mitochondrial disease 1: Institute of Neurosciences, Autonomous University of Barcelona, Barcelona, Spain; 2: Department of Cell Biology, Physiology and Immunology, Autonomous University of Barcelona, Barcelona, Spain; 3: Clinical Neuroproteomics Unit, Navarrabiomed, Complejo Hospitalario de Navarra (CHN), Universidad Pública de Navarra (UPNA), Pamplona, Spain; 4: Centro de Análisis Genómico, CNAG-CRG, Barcelona, Spain Oral presentation The contribution of cell free-mitochondrial DNA in the pathogenesis of MELAS syndrome 1: IRCCS Istituto delle Scienze Neurologiche di Bologna, Programma di Neurogenetica, Italy; 2: Department of Biomedical and NeuroMotor Sciences, University of Bologna, Italy Oral presentation A novel role for the mitochondrial topoisomerase TOP1MT in mediating mtDNA release and cGAS-STING activation 1: University of Calgary, Canada; 2: National Institutes of Health; 3: Texas A&M University; 4: University of British Columbia Flash Talk Impaired inflammatory response to lipopolysaccharide in fibroblasts from patients with long-chain fatty acid oxidation disorders 1: Laboratory Genetic Metabolic Diseases, Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands; 2: Research Unit for Molecular Medicine, Department of Clinical Medicine, Aarhus University and Aarhus University Hospital, Aarhus, Denmark; 3: Department of Biomedicine, Aarhus Research Center for Innate Immunology, Aarhus University, Aarhus, Denmark; 4: Department of Experimental Vascular Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands; 5: Core Facility Metabolomics, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, The Netherlands Flash Talk Fumarate induces mtDNA release via mitochondrial-derived vesicles and drives innate immunity 1: Medical Research Council, MBU,University of Cambridge, UK; 2: Medical Research Council Cancer Unit,University of Cambridge, UK; 3: CECAD Research Centre, University of Cologne, Cologne, Germany Flash Talk Free cytosolic-mitochondrial DNA triggers a potent type-I Interferon response in Kearns–Sayre patients counteracted by mofetil mycophenolate 1: Unit of Cellular Biology and Diagnosis of Mitochondrial Diseases, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy; 2: Division of Rheumatology, Bambino Gesù Children’s Hospital, IRCCS, Rome, Italy; 3: Division of Metabolism, Bambino Gesù Children’s Hospital, IRCCS, Rome, Italy; 4: Research Unit of Muscular and Neurodegenerative Disorders, Bambino Gesù Children’s Hospital, IRCCS, Rome, Italy |
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10:45am - 11:00am |
Coffee Break Location: Bologna Congress Center |
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11:00am - 12:40pm |
Session 3.2: Mitochondrial mechanisms in neurodegeneration and neurodevelopment Location: Bologna Congress Center - Sala Europa Chair: Vincent Procaccio Chair: Elena Rugarli Invited Speaker: V. Paquis-Flucklinger; L. Burbulla
Destructuring of mitochondrial cristae in the initiation of CHCHD10-related neurodegeneration 1: IRCAN, UMR 7284/INSERM U1081/UCA, Nice, France; 2: Reference Center for mitochondrial diseases, Universitary hospital, Nice, France Invited Convergence of mitochondrial and lysosomal dysfunction in Parkinson’s disease Ludwig Maximilian University (LMU) Munich, Germany Oral presentation Development of cortical organoids to model m.3243A>G disease and understand cell specificity University of Cambridge, United Kingdom Oral presentation Brain and brainstem-specific mitochondrial diversity associated with vulnerability to neurodegeneration in mitochondrial diseases 1: Division of Behavioral Medicine, Department of Psychiatry, Columbia University Irving Medical Center, New York NY, USA; 2: Center for Translational & Computational Neuroimmunology, Department of Neurology and the Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, Columbia University Irving Medical Center, New York NY, USA; 3: Division of Molecular Therapeutics, Department of Psychiatry, Columbia University Irving Medical Center, New York NY, USA; 4: Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL, USA; 5: Department of Neurological Sciences, Rush University Medical Center, Chicago, IL, USA; 6: New York State Psychiatric Institute, New York NY, USA; 7: Department of Neurology, Columbia University Irving Medical Center, New York NY, USA Oral presentation Mitochondrial DNA mutations exacerbate motor and behavioural deficits in a mouse model of Parkinson’s disease 1: Clinical and Translational Research Institute, Centre for Life, Newcastle University, UK, NE3 1BZ; 2: Department of Clinical Neuroscience, University of Cambridge, UK, CB2 0QQ; 3: Medical Research Council Mitochondrial Biology Unit, University of Cambridge, UK, CB2 0QQ; 4: Division of Molecular Metabolism, Biomedicum, floor 9D, Solnavägen 9, Karlolinska Institute, 171 65 Stockholm, Sweden; 5: Newcastle Magnetic Resonance Centre, Campus for Ageing and Vitality, Newcastle University, NE4 5PL Flash Talk Macromolecular crowding: A novel player in mitochondrial physiology and disease 1: Radboud University Medical Center, The Netherlands; 2: University of Amsterdam, The Netherlands; 3: King's College, London, UK; 4: University of Twente, The Netherlands; 5: Wageningen University, The Netherlands Flash Talk Preserved motor function and striatal innervation despite severe degeneration of dopamine neurons upon mitochondrial dysfunction 1: Center for Physiology and Pathophysiology, Faculty of Medicine and University Hospital Cologne, Germany; 2: Medical Research Council Mitochondrial Biology Unit, University of Cambridge, UK; 3: Medical Research Council Mitochondrial Biology Unit and Department of Clinical Neurosciences, Cambridge Biomedical Campus, University of Cambridge, UK; 4: Department of Neurology, Faculty of Medicine and University Hospital Cologne, Germany; 5: Institute of Radiochemistry and Experiment Molecular Imaging, Faculty of Medicine and University Hospital of Cologne, Germany; 6: Department of Pediatrics and Adolescent Medicine, Experimental Neonatology, Faculty of Medicine and University Hospital Cologne, Germany; 7: Center for Physiology and Pathophysiology, Faculty of Medicine and University Hospital Cologne; Cologne Excellence Cluster on Cellular Stress Responses in Aging-associated Diseases (CECAD) and Center for Molecular Medicine Cologne, University of Cologne, Germany Flash Talk The mitochondrial DNA depletion syndrome protein FBXL4 mediates the degradation of the mitophagy receptors BNIP3 and NIX to suppress mitophagy 1: School of Biomedical Sciences, Faculty of Medicine, University of Queensland, Brisbane, Australia; 2: Department of Biotechnology, School of Biotechnology, Viet Nam National University-International University, Ho Chi Minh City, Vietnam; 3: Department of Biochemistry and Molecular Pharmacology, New York University Grossman School of Medicine, New York, USA; 4: Perlmutter Cancer Center, New York University Grossman School of Medicine, New York, USA; 5: The University of Queensland, Institute for Molecular Bioscience, Brisbane, Australia; 6: Wellcome Centre for Mitochondrial Research, Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK; 7: NHS Highly Specialised Service for Rare Mitochondrial Disorders, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK; 8: The University of Queensland Diamantina Institute, Faculty of Medicine, The University of Queensland, Brisbane, Australia |
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12:40pm - 12:45pm |
Conference Picture Location: Bologna Congress Center - Sala Europa |
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12:45pm - 1:15pm |
Industry Workshop: Oroboros Location: Bologna Congress Center - Sala Europa |
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12:45pm - 1:45pm |
Lunch Location: Bologna Congress Center - Sala Europa |
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1:45pm - 3:30pm |
Session 3.3: Metabolic stress responses in mitochondrial diseases and cancer Location: Bologna Congress Center - Sala Europa Chair: Luca Scorrano Chair: Luisa Iommarini Invited Speaker: A. Trifunovic; L. Greaves
Transcriptional regulation of mitochondrial stress responses University of Cologne, Germany Invited Mitochondrial DNA mutations in ageing and cancer - what's the connection? 1: Wellcome Centre for Mitochondrial Research, Newcastle University, United Kingdom; 2: MRC Mitochondrial Biology Unit, Cambridge, United Kingdom; 3: CRUK Beatson Institute, Glasgow, United Kingdom Oral presentation Mitochondrial complex III deficiency drives c-MYC overexpression and illicit cell cycle entry leading to senescence and segmental progeria 1: Folkhälsan Research Center, Finland; 2: Stem Cells and Metabolism Research Program, Faculty of Medicine, University of Helsinki, Finland; 3: Viikki Metabolomics Unit, University of Helsinki, Finland; 4: Division of Infection Medicine, Department of Clinical Sciences, Lund University, Sweden; 5: Colzyx AB, Lund, Sweden; 6: Department of Clinical Sciences, Lund, Pediatrics, Lund University, Sweden; 7: Children’s Hospital, Helsinki University Hospital, Finland Oral presentation A genetic deficiency screen in vivo reveals rescue mechanisms of mitochondrial dysfunction 1: Karolinska Institutet, Sweden; 2: Max-Planck Institute of Biochemistry, Germany; 3: University of Cambridge, Cambridge Biomedical Campus, UK Oral presentation Heterochromatin Protein 1 controls gene expression and longevity in response to mitochondrial dysfunction 1: Andalusian Centre for Developmental Biology (CABD). CSIC-Universidad Pablo de Olavide-Junta de Andalucía. Carretera de Utrera Km 1, 41013 Sevilla, Spain.; 2: Department of Molecular Biology and Biochemical Engineering, Universidad Pablo de Olavide. Carretera de Utrera Km 1, 41013 Seville, Spain; 3: Department of Biochemistry, Medical School, Kochi University, Kohasu, Oko-cho, Nankoku, Kochi 783-8505, Japan. Flash Talk High fat diet ameliorates the mitochondrial cardiomyopathy of CHCHD10 mutant mice Weill Cornell Medicine, United States of America Flash Talk Functional characterisation of the human mitochondrial disaggregase, CLPB 1: Department of Biochemistry and Pharmacology, The Bio21 Molecular Science and Biotechnology Institute, The University of Melbourne, Parkville VIC 3010, Australia; 2: Murdoch Children’s Research Institute, Royal Children’s Hospital and Department of Paediatrics, The University of Melbourne, Parkville VIC 3052, Australia; 3: Victorian Clinical Genetics Services, Royal Children’s Hospital, Melbourne, Parkville VIC 3052, Australia Flash Talk The mitochondrial inhibitor IF1 has a dual role in cancer 1: Department of Biomedical and Neuromotor Sciences, University of Bologna; 2: Department of Chemical Science, University of Padova; 3: Department of Biology, University of Padova, Padova |
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3:30pm - 3:50pm |
Industry Workshop: UCB Farchim SA Location: Bologna Congress Center - Sala Europa |
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3:30pm - 4:30pm |
Tea Break and poster session Location: Bologna Congress Center Session topics:
- Clinical 2: natural history, biomarkers and outcome measures - Inflammation and Immunity as mitochondrial contributor to pathology - Metabolic stress responses in mitochondrial diseases, ageing and cancer Evaluating functional mobility and endurance in adults with Primary Mitochondrial Myopathy (PMM); insights concerning gait protocol and outcome measure selection. 1: Translational and Clinical Research Institute, Newcastle University, UK; 2: National Institute for Health and Care Research (NIHR) Newcastle Biomedical Research Centre (BRC), Newcastle University and The Newcastle upon Tyne Hospitals NHS Foundation Trust, UK; 3: Newcastle Clinical Trials Unit, Newcastle University, UK; 4: Population Health Sciences Institute, Newcastle University, UK; 5: Pharmacy Directorate, The Newcastle upon Tyne Hospitals NHS Foundation Trust, UK; 6: The Newcastle upon Tyne Hospitals NHS Foundation Trust, UK; 7: Wellcome Centre for Mitochondrial Research, Translational and Clinical Research Institute, Newcastle University, UK; 8: NHS Highly Specialised Service for Rare Mitochondrial Disorders, The Newcastle upon Tyne Hospitals NHS Foundation Trust, UK Natural variability in protein expression of oxidative deficiency markers in single muscle fibres and tissue homogenate mitochondrial genetics in m.3243A>G-related myopathy 1: Wellcome Centre for Mitochondrial Research, Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, United Kingdom; 2: NHS Highly Specialised Service for Rare Mitochondrial Disorders, Newcastle upon Tyne, United Kingdom; 3: Centre for Doctoral Training in Cloud Computing and Big Data, Newcastle upon Tyne, United Kingdom Retrospective natural history of mitochondrial deoxyguanosine kinase deficiency: a worldwide cohort of 197 patients 1: Department of Medical and Surgical Sciences, Alma Mater Studiorum University of Bologna; 2: IRCCS Istituto delle Scienze Neurologiche, Neuropsichiatria dell’età pediatrica, Bologna; 3: Department of Biochemistry, Bicêtre Hospital, Reference Center for Mitochondrial Disease, University of Paris-Saclay, Assistance Publique-Hôpitaux de Paris, France; 4: School of Medicine, Institute of Human Genetics, Technical University of Munich,Germany; 5: Institute of Neurogenomics, Computational Health Center, Helmholtz Zentrum München, Neuherberg, Germany; 6: H. Houston Merritt Neuromuscular Research Center, Department of Neurology, Columbia University Irving Medical Center, New York, NY, USA; 7: Dino Ferrari Center, Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy; 8: Pediatric Hepatology and Pediatric Liver Transplantation Unit, Bicêtre Hospital, Reference Center for Mitochondrial Disease, University of Paris-Saclay, Assistance Publique-Hôpitaux de Paris, Paris, France; 9: Center for Medical Genetics, Department of Metabolism, Chiba Children's Hospital, 579-1 Heta-cho, Midori-ku, Chiba, 266-000, Japan; 10: Diagnostics and Therapeutic of Intractable Diseases, Intractable Disease Research Center, Graduate School of Medicine, Juntendo University, Hongo 2-1-1, Bunkyo-ku, Tokyo, 113-8421, Japan; 11: Department of Pediatrics, University Hospital Centre Zagreb, Zagreb, Croatia; 12: Clinic for Pediatrics, Division of Inherited Metabolic Disorders, Medical University of Innsbruck, 6020 Innsbruck, Austria; 13: University Children's Hospital, Paracelsus Medical University (PMU), 5020 Salzburg, Austria; 14: Division of Metabolism, Bambino Gesù Children's Hospital IRCCS, Rome, Italy; 15: Department of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy; 16: IRCCS Istituto di Scienze Neurologiche di Bologna, Programma di Neurogenetica, Bologna, Italy; 17: Dipartimento di Neuroscienze, Organi di Senso e Torace, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, Italy.; 18: Dipartimento Di Neuroscienze, Università Cattolica del Sacro Cuore, Rome, Italy.; 19: Department of Pediatrics, University Medical Center Hamburg Eppendorf, Hamburg, Germany; 20: MitoLab, UMR CNRS 6015 - INSERM U1083, MitoVasc Institute , Angers University Hospital, Angers, France; 21: Centre de référence des maladies héréditaires du métabolisme, CHU la Timone Enfants, Marseille, France; 22: Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Regional Clinical Center for expanded newborn screening, Milan, Italy; 23: Department of Pediatrics, Fondazione IRCCS San Gerardo dei Tintori, 20900 Monza, Italy.; 24: Unité de Gastroentérologie, Hépatologie, Nutrition et Maladies Héréditaires du Métabolisme, Hôpital des Enfants, CHU de Toulouse, Toulouse, France; 25: Division of Medical Genetics and Neurogenetics, Fondazione IRCCS Neurological Institute "C. Besta", Milan, Italy; 26: Division of Neuropaediatrics and Paediatric Metabolic Medicine, Center for Paediatric and Adolescent Medicine, University Hospital Heidelberg, Heidelberg, Germany; 27: Department of Clinical and Experimental Medicine, Neurological Institute, University of Pisa & AOUP, Italy; 28: Unit of Neurology and Neuromuscular Disorders, Department of Clinical and experimental Medicine, University of Messina, Italy; 29: Department of Paediatrics, Medical Sciences Division, Oxford University, Oxford OX3 9DU, UK; 30: Metabolic Unit, Meyer Children's Hospital IRCCS, Florence, Italy; 31: Centre de référence des Maladies Mitochondriales, Service de Génétique Médicale, CHU de Nice, Université Côte d’Azur, CNRS, INSERM, IRCAN, Nice, France; 32: Department of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, University College London, London, United Kingdom; 33: Metabolic Clinic, Ruth Rappaport Children's Hospital, Rambam Health Care Campus, Haifa, Israel Tissue, molecular and metabolic changes in the liver of patients with Mitochondrial Neurogastrointestinal Encephalomyopathy 1: Department of Biomedical and NeuroMotor Sciences (DIBINEM), University of Bologna, Bologna, Italy; 2: IRCCS Istituto delle Scienze Neurologiche di Bologna. Italy; 3: Department of Life Quality Studies (QuVI), University of Bologna, Bologna, Italy; 4: University Hospital Vall d'Hebron. Barcelona. Spain; 5: IRCCS St. Orsola. Bologna. Italy; 6: Department of Translational Medicine, University of Ferrara, Ferrara, Italy Phenotyping mtDNA-related diseases in childhood: a cohort study of 150 patients Fondazione IRCCS Besta, Milan Italy Carrier frequency of pathogenic and likely pathogenic variants in POLG in Eastern Norway 1: Department of Medical Genetics, Oslo University Hospital, Oslo, Norway; 2: Department of Medical Biochemistry, Oslo University Hospital, Oslo, Norway; 3: Department of Clinical Medicine (K1), University of Bergen, Bergen, Norway; 4: Department of Medical Genetics, Haukeland University Hospital, Bergen, Norway; 5: Department of Medical Genetics, Telemark Hospital Trust, Skien, Norway; 6: Metabolic Unit, Great Ormond Street Hospital, London, UK.; 7: Mitochondrial Research Group, Genetics and Genomic Medicine Department, UCL Great Ormond Street Institute of Child Health, London, UK.; 8: Department of Neurology, Haukeland University Hospital, Bergen, Norway; 9: Nasjonal kompetansetjeneste for medfødte stoffskiftesykdommer, Oslo University Hospital, Oslo, Norway; 10: Department of Pediatrics, Haukeland University Hospital, Bergen, Norway Exercise testing and measurement of habitual physical activities in m.3243A>G-related Mitochondrial Disease 1: Wellcome Centre for Mitochondrial Research. Clinical and Translational Research Institute. Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, United Kingdom; 2: NHS Highly Specialised Service for Rare Mitochondrial Disorders of Adults and Children, Newcastle upon Tyne Hospitals NHS Foundation Trust Leber’s hereditary optic neuropathy in females. 1: Dipartimento di Scienze Biomediche e Neuromotorie, University of Bologna, Italy; 2: IRCCS Istituto delle Scienze Neurologiche di Bologna, Programma di Neurogenetica, Bologna, Italy; 3: IRCCS Istituto delle Scienze Neurologiche di Bologna, UOC Clinica Neurologica, Bologna, Italy Non-invasive tool for mitochondrial diseases diagnostics 1: Laboratory of Bioenergetics, Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic; 2: 1st Faculty of medicine, Charles University, Prague, Czech Republic Obstetric history of women with m.3243A>G – a retrospective cohort study University of Oulu and Oulu University Hospital, Finland Clustering analysis with optical coherence tomography data in Leber hereditary optic neuropathy (LHON) patients by non-negative matrix factorization unsupervised learning technique 1: IRCCS Istituto delle Scienze Neurologiche di Bologna, Programma di Neurogenetica - Bologna (Italy); 2: Dipartimento di Scienze Biomediche e Neuromotorie, Università di Bologna - Bologna (Italy); 3: IRCCS Istituto delle Scienze Neurologiche di Bologna, UOC Clinica Neurologica - Bologna (Italy); 4: Department of Ophthalmology, University Vita-Salute, IRCCS Ospedale San Raffaele – Milan (Italy); 5: Studio Oculistico d’Azeglio - Bologna (Italy) Leigh syndrome global patient registry - cure mito foundation 1: Cure Mito Foundation, United States of America; 2: Cure Mito Foundation, United States of America; 3: Cure Mito Foundation, United States of America; Johns Hopkins University School of Medicine; 4: Cure Mito Foundation, United States of America; 5: Cure Mito Foundation, United States of America; 6: Perot Foundation Neuroscience Transla-tional Research Center (PNTRC), The University of Texas Southwestern Medical Center O'Donnell Brain Institute; 7: Midwestern University College of Pharmacy; 8: Midwestern University College of Pharmacy; 9: Cure Mito Foundation; The University of Texas Southwestern Medical Center Mitochondrial ATP synthase deficiency and its relationship with the urea cycle 1: Division of Metabolism, Department of Pediatric Subspecialties, Bambino Gesù Children's Hospital, Rome, Italy; 2: Laboratory of Metabolic Diseases, Bambino Gesù Children's Hospital, IRCCS, 00146 Rome, Italy; 3: Unit of Muscular and Neurodegenerative Disorders, Laboratory of Molecular Medicine, Bambino Gesù Children’s Hospital, IRCCS, Rome, Italy Quantifying ataxia in adult patients with primary mitochondrial disease 1: Wellcome Centre for Mitochondrial Research, Newcastle University, United Kingdom; 2: NIHR Newcastle Biomedical Research Centre, Newcastle University; 3: NHS Highly Specialised Service for Rare Mitochondrial Disorders, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK; 4: Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK Retrospective natural history study of MTRFR/C12orf65-related disorders 1: East Anglian Medical Genetics Service, Cambridge University Hospitals NHS Foundation Trust, Cambridge, United Kingdom; 2: Department of Clinical Neurosciences, University of Cambridge, Cambridge, United Kingdom (add-tr.mitoteam@nhs.net); 3: Hereditary Neuropathy Foundation, New York, NY, USA (https://www.hnf-cure.org/) Correlation of mitochondrial respiration in platelets, peripheral blood mononuclear cells and muscle fibres 1: Lund University, Sweden; 2: A&E Department, Kungälv Hospital, Kungälv, Sweden; 3: Children's Medical Center, Landspitali-The National University Hospital of Iceland, Reykjavík, Iceland; 4: Department of Neurosurgery, Rigshospitalet, Copenhagen, Denmark; 5: Skåne University Hospital, Department of Intensive- and perioperative Care, Malmö, Sweden; 6: Department of Pediatrics, Skåne University Hospital, Lund University, Lund, Sweden; 7: Clinical Physiology, Department of Clinical Sciences Lund, Lund University, Skåne University Hospital, Lund, Sweden; 8: Department of Pediatrics, The Queen Silvia Children’s Hospital, University of Gothenburg, Gothenburg, Sweden; 9: Lund University, Department of Clinical Sciences Lund, Translational Neurology Group and Wallenberg Center for Molecular Medicine, Lund, Sweden; 10: Lund University, Skåne University Hospital, Department of Clinical Sciences Lund, Otorhinolaryngology, Head and Neck Surgery, Lund, Sweden Epidemiology and the natural history of POLG disease in Norway 1: Department of Medical Biochemistry, Oslo University Hospital, Norway; 2: Department of Clinical Medicine (K1), University of Bergen, Norway; 3: Department of Medical Genetics, Oslo University Hospital, Norway; 4: Department of Medical Genetics, Haukeland University Hospital, Norway; 5: Paediatric Research Group, Department of Clinical Medicine, UiT The Artic University of Norway, Norway; 6: Department of Paediatrics, University Hospital of North Norway, Norway; 7: Department of Neurology, St. Olav’s Hospital, University Hospital, Norway; 8: Department of Neuroscience and Movement Science, Faculty of Medicine, Norwegian University of Science and Technology, Norway; 9: Unit for Congenital and Hereditary Neuromuscular Conditions (EMAN), Department of Neurology, Oslo University Hospital, Norway; 10: Department of Clinical Neurosciences for Children, Oslo University Hospital, Norway; 11: Norwegian National Unit for Newborn Screening, Division of Paediatric and Adolescent Medicine, Oslo University Hospital, Norway. European Reference Network for Hereditary Metabolic Disorders; 12: Metabolic Unit, Great Ormond Street Hospital, London, UK. European Reference Network for Hereditary Metabolic Disorders; 13: Mitochondrial Research Group, Genetics and Genomic Medicine Department, UCL Great Ormond Street Institute of Child Health, UK; 14: Department of Neurology, Haukeland University Hospital, Norway; 15: Department of Pediatrics, Haukeland University Hospital, Norway The evolving phenotypic profile of cardiomyopathy in patients with Barth syndrome 1: Medical University of South Carolina, Charleston, SC, United States of America; 2: Department of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, United States of America; 3: Henry Ford Hospital, Detroit, MI, United States of America; 4: Stealth BioTherapeutics, Inc, Needham, MA, United States of America True or false mitochondrial disorder? 1: INSERM UMR1163, Université Sorbonne Paris Cité, Institut Imagine, 75015 Paris, France; 2: Departments of Pediatric and Genetics, Hôpital Necker-Enfants-Malades, Paris, France; 3: CARAMMEL reference center for mitochondrial diseases An automated processing pipeline to perform probabilistic tractography of the anterior optic pathway applied to Leber’s hereditary optic neuropathy. 1: Department of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy; 2: IRCCS Istituto delle Scienze Neurologiche di Bologna, Italy; 3: Department of Physics and Astronomy, University of Bologna, Bologna, Italy Natural history of Pearson syndrome: various clinical courses with changes in clinical phenotypes 1: Department of Paediatrics and Adolescent Medicine, Division of Paediatric Haematology and Oncology, Medical Center, Faculty of Medicine, University of Freiburg, Germany; 2: Department of General Paediatrics, Adolescent Medicine and Neonatology, Faculty of Medicine, University Medical Center, University of Freiburg, Freiburg, Germany; 3: Department of Paediatric Oncology, Haematology and Clinical Immunology, Medical Faculty, Heinrich Heine University, Duesseldorf, Germany; 4: Department of Paediatrics and Adolescent Medicine, University Medical Center Ulm, Ulm, Germany; 5: Medical University of Innsbruck, Clinic for Paediatrics, Inherited Metabolic Disorders, Innsbruck, Austria Phenotype and natural history of pantothenate kinase-associated neurodegeneration (PKAN) 1: Department of Neurology With Friedrich Baur Institute, University Hospital of Ludwig-Maximilians-Universität München, Munich, Germany; 2: German Center for Neurodegenerative Diseases (DZNE), Munich, Germany; 3: Munich Cluster for Systems Neurology, Munich, Germany RARS2 disease’s morbidity and mortality correlate with the severity of brain involvement 1: Department of Medical and Surgical Sciences, Alma Mater Studiorum University of Bologna, Bologna, Italy; 2: IRCCS Istituto delle Scienze Neurologiche di Bologna, Neuropsichiatria dell’età pediatrica, Bologna, Italy; 3: Dipartimento di Scienze Biomediche e Neuromotorie, Alma Mater Studiorum University of Bologna, Bologna, Italy; 4: IRCCS Istituto delle Scienze Neurologiche di Bologna, Programma di Neurogenetica, Bologna, Italy A new non-invasive diagnostic method for detection of pathogenic mitochondrial DNA variants using faecal-derived DNA samples. 1: Wellcome Centre for Mitochondrial Research, Translational and Clinical Research Institute; NIHR Newcastle Biomedical Research Centre, Newcastle University, Newcastle upon Tyne NE2 4HH, UK; 2: Department of Neurosciences, NHS Highly Specialised Service for Rare Mitochondrial Disorders, Newcastle upon Tyne NE2 4HH, UK Complex V assembly intermediates in human muscle from patient with suspected mitochondrial disease - Potential insights into disease mechanisms. 1: Neurometabolic Unit, NHNN, University College London Hospitals; 2: Chemical Pathology Laboratory, Great Ormond Street Hospital for Children; 3: Queen Square Institute of Neurology, University College London; 4: Great Ormond Street Institute of Child Health, University College London Prolonged gastrointestinal transit times in mitochondrial disease – a case control study 1: Dept. of Clinical Genetics, Aalborg University Hospital, Aalborg, Denmark; 2: Dept.of Clinical Medicine, Aalborg University, Aalborg, Denmark; 3: Mech-Sense, Dept. of Gastroenterology, Aalborg University Hospital, Aalborg, Denmark; 4: Dept. of Molecular Diagnostics, Aalborg University Hospital, Aalborg, Denmark Rethinking mitochondrial diabetes: a multifaceted disease entity 1: Department of Neuromuscular Diseases, UCL Queen Square Institute of Neurology, London, UK; 2: NHS Highly Specialised Service for Rare Mitochondrial Disorders, Queen Square Centre for Neuromuscular Diseases, The National Hospital for Neurology and Neurosurgery, London, UK; 3: Endocrinology Department, University College London Hospital, London, UK Therapeutic intervention in Leber Hereditary Optic Neuropathy: later is better? 1: IRCCS Istituto delle Scienze Neurologiche di Bologna, Programma di Neurogenetica - Bologna (Italy); 2: Dipartimento di Scienze Biomediche e Neuromotorie, Università di Bologna - Bologna (Italy); 3: IRCCS Istituto delle Scienze Neurologiche di Bologna, UOC Clinica Neurologica - Bologna (Italy); 4: Department ofOphthalmology, University Vita-Salute, IRCCS Ospedale San Raffaele – Milan (Italy); 5: Studio Oculistico d’Azeglio - Bologna (Italy) Neurofilament light chain – an emerging biomarker in mitochondrial disease 1: IRCCS Istituto delle Scienze Neurologiche di Bologna, Bologna, Italy.; 2: Department of Biomedical and Neuromotor Sciences, University of Bologna,; 3: Department of Clinical Medicine (K1), University of Bergen, Bergen, Norway; 4: Dept. of Neurology, Haukeland University Hospital, Norway; 5: Neuro-SysMed - Centre of Excellence for Experimental Therapy in Neurology, Departments of Neurology and Clinical Medicine, Bergen, Norway Assessing the role of mtdsRNA as a trigger for neuroinflammation in a mouse model of Leigh syndrome 1: Institute of Neurosciences, Autonomous University of Barcelona, Barcelona, Spain; 2: Department of Cell Biology, Physiology and Immunology, Autonomous University of Barcelona, Barcelona, Spain Concerted cell-specific neuronal programs drive neurodegeneration in Leigh Syndrome Universitat Autònoma de Barcelona, Spain Parkinson’s disease genes converge at the mitochondria-lysosome interface to promote inflammatory cell death McGill University, Canada [18F]ROStrace PET as a biomarker of mitochondria-induced neuroinflammation in the prodromal phase of Parkinson’s disease mouse models 1: Children's Hospital of Philadelphia, United States of America; 2: University of Pennsylvania, United States of America Modulation of immune cell activation and differentiation by mitochondrial nicotinamide adenine dinucleotide levels 1: Instituto Universitario de Biología Molecular – UAM (IUBM-UAM), Departamento de Biología Molecular, Universidad Autónoma de Madrid, 28049 Madrid, Spain; 2: Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas - Universidad Autónoma de Madrid (CSIC-UAM), 28049 Madrid, Spain MtDNA replication stress and innate immune signalling Max Planck Institute for Biology of Ageing, Germany Inflammatory cardiomyopathy and heart failure caused by impaired inner membrane integrity 1: Institut Pasteur, Mitochondrial Biology Group, CNRS UMR 3691, Université Paris Cité, Paris, France; 2: Department of Translational Research, Comprehensive Heart Failure Center (CHFC), Medical Clinic 1, University ClinicWürzburg,Würzburg, Germany; 3: Institut Pasteur, Biomics Technological Platform, Université Paris Cité, Paris, France; 4: Institut Pasteur, Proteomics Core Facility, MSBio UtechS, UAR CNRS 2024, Université Paris Cité, Paris, France Lack of SIRT3 results in a constitutive IFNbeta release and protects against viral infection 1: Instituto Universitario de Biología Molecular – UAM (IUBM-UAM), Departamento de Biología Molecular, Universidad Autónoma de Madrid, 28049 Madrid, Spain; 2: Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas - Universidad Autónoma de Madrid (CSIC-UAM), 28049 Madrid, Spain Mitochondrial DNA variation alters cell-mediated and humoral innate immune responses 1: Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland; 2: Institute of Evolutionary Biology, School of Biological Sciences, University of Edinburgh, UK Iron homeostasis in mitochondria is critical for the survival of T cells University of Michigan, United States of America Inflammatory conditions, redox status and c-miRNAs as potential predictors of vascular damage in type 2 diabetes mellitus patients. 1: Department of Biochemistry and Molecular Biology I, Faculty of Science, University of Granada, Spain; 2: Institute of Biotechnology, Biomedical Research Center, Health Sciences Technology Park, University of Granada, Granada, Spain; 3: Centro de Investigación Biomédica en Red Fragilidad y Envejecimiento Saludable (CIBERFES), Instituto de Investigación Biosanitaria (Ibs), Granada, San Cecilio University Hospital, Granada, Spain; 4: Department of Biophysics, Biomedicine and Neuroscience, Al-Farabi Kazakh National University, Almaty, Kazakhstan; 5: Departamento de Investigación y Extensión, Centro de Enseñanza Técnica Industrial; Guadalajara, Jalisco, México; 6: Hospital de Alcalá la Real, Andalucia, Spain; 7: Endocrinology and Nutrition Unit, Instituto de Investigación Biosanitaria de Granada (Ibs.GRANADA), University Hospital Clínico San Cecilio, Granada, Spain.; 8: Department of Physiology, Faculty of Medicine, University of Granada. Loss of pathogenic mitochondrial tRNA mutations during the development of adaptive immune responses 1: Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm 17165, Sweden; 2: Max Planck Institute Biology of Ageing-Karolinska Institutet Laboratory, Karolinska Institutet, Stockholm 17165, Sweden.; 3: Applied Immunology and Immunotherapy, Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska University Hospital, Stockholm 17176, Sweden; 4: Center for Inherited Metabolic Diseases, Karolinska University Hospital, Stockholm 17164, Sweden.; 5: Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm 17177, Sweden. Role of mitochondrial dynamics in abdominal aortic aneurysm 1: UMR CNRS 6015, INSERM U1083, MitoVasc Institute, CarMe Team, University of Angers, France; 2: CHU of Angers, France Between benefit and harm – the effect of antibiotics-induced mitochondrial stress on innate immune responses Tampere University, Finland Mitochondrial thermo-profiles of diverse cell lines show reduction of thermo-stability at pathophysiological conditions 1: Tampere University, Finland; 2: University of Copenhagen; 3: Osaka University Mitochondrial thermogenesis and thermal adaptation in fibroblasts 1: Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland; 2: Department of Environmental and Biological Sciences, University of Eastern Finland, Joensuu, Finland Effects of SIRT1 modulators in a pregnancy-induced mouse model of primary mitochondrial cardiomyopathy 1: Neuroscience Graduate Program, Will Cornell Graduate School of Medical Sciences, 1300 York Ave, New York, NY 10065, USA; 2: Feil Family Brain and Mind Research Institute, Weill Cornell Medicine, 407 East 61st Street, New York, NY 10065, USA.; 3: Elysium Health New York, New York, NY 10013, USA A common genetic variant of a mitochondrial RNA processing enzyme predisposes to insulin resistance 1: Harry Perkins Institute of Medical Research, Nedlands, Western Australia 6009, Australia; 2: ARC Centre of Excellence in Synthetic Biology, QEII Medical Centre, Nedlands, Western Australia 6009, Australia; 3: Centre for Medical Research, The University of Western Australia, QEII Medical Centre, Nedlands, Western Australia 6009, Australia.; 4: Max Planck Institute for Biology of Ageing, D-50931 Cologne, Germany; 5: Faculty of Health and Medical Sciences, Medical School, The Rural Clinical School of Western Australia, The University of Western Australia, Bunbury, Western Australia 6230, Australia; 6: Department of Anatomy and Embryology, Faculty of Medicine, Laboratory Animal Resource Center (LARC), and Transborder Medical Research Center, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan; 7: Dobney Hypertension Centre, Medical School, The University of Western Australia, Perth, Western Australia, Australia; 8: Australian National Phenome Centre, Centre for Computational and Systems Medicine, Health Futures Institute, Murdoch University, Harry Perkins Building, Perth, Western Australia 6150, Australia; 9: School of Human Sciences (Physiology), The University of Western Australia, Crawley, Western Australia 6009, Australia.; 10: Victor Chang Cardiac Research Institute, Darlinghurst, Sydney, New South Wales 2010, Australia.; 11: Curtin Medical School, Curtin University, Bentley, Western Australia 6102, Australia; 12: Curtin Health Innovation Research Institute, Curtin University, Bentley, Western Australia 6102, Australia.; 13: Telethon Kids Institute, Northern Entrance, Perth Children's Hospital, 15 Hospital Avenue, Nedlands, Western Australia, Australia. Metformin enhanced the Effect of Ketogenic Diet and low Dose of Cyclophosphamide in MYCN-amplified Neuroblastoma 1: Paracelsus Medical University, Austria; 2: Shuzhao Li Lab The Jackson Laboratory for Genomic Medicine, Farmington, USA; 3: Spinal Cord Injury and Tissue Regeneration Center Salzburg (SCI-TReCS), Cell Therapy Institute; 4: Core Facilities, Medical University of Vienna, Vienna, Austria Respiratory complex I deficiency triggers integrated stress response upon metabolic challenge 1: University of Bologna, Department of Pharmacy and Biotechnology, Italy; 2: University of Bologna, Department of Medical and Surgical Sciences, Italy; 3: University of Bologna, Department of Biomedical and Neuromotor Sciences, Italy; 4: University of Padua, Department of Biomedical Sciences, Italy Stress responses in a novel mitochondrial myopathy mouse model Bogazici University, Turkey The multifaceted role of GDF15 in mitochondrial muscle disease and its synergistic action with FGF21 1: University of Helsinki, Finland; 2: Nadmed Ltd, Helsinki, Finland; 3: NGM Biopharmaceuticals, South San Francisco, CA 94080, USA Red 630 light transcranial LED therapy (RL-TCLT) stimulates bioenergetic mitochondrial function, enhancing neuronal arborization and reducing hippocampal memory loss in aged SAMP8 mice. 1: Neurobiology of Aging Lab, CEBICEM, Universidad San Sebastián, Chile; 2: Centro Ciencia & Vida, Fundación Ciencia & Vida, Chile.; 3: Escuela de Ingeniería Civil Biomédica, Universidad de Valparaíso, Chile. The mitokine GDF15 correlates with differentially dietary fat intake in pregnancies with intrauterine growth restriction 1: Inherited metabolic diseases and muscular disorders Lab, Cellex - Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Faculty of Medicine and Health Science - University of Barcelona (UB), 08036 Barcelona, Spain; 2: Internal Medicine Unit, Hospital Clínic of Barcelona, 08036 Barcelona, Spain; 3: Biomedical Network Research Centre on Rare Diseases (CIBERER), Instituto de Salud Carlos III, 28029 Madrid, Spain; 4: BCNatal—Barcelona Centre for Maternal-Foetal and Neonatal Medicine (Hospital Clínic and Hospital Sant Joan de Déu), IDIBAPS, University of Barcelona, 08036 Barcelona, Spain; 5: Medicine Department, Faculty of Medicine. CIBEROBN Obesity and Nutrition Physiopathology. Institut de Recerca en Nutrició i Seguretat Alimentaria (INSA-UB). University of Barcelona, Barcelona, Spain. Fundación Dieta Mediterránea, Barcelona, Spain, Telomerase is crucial for mitochondrial function in human cardiomyocytes 1: Institute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Hannover, Germany; 2: REBIRTH Center for Translational Regenerative Medicine, Hannover Medical School, Hannover, Germany; 3: Fraunhofer Institute for Toxicology and Experimental Medicine, Hannover, Germany Drug repositioning as a mitochondrial-targeted therapeutic approach for neurodegenerations associated with OPA1 mutations 1: Dept. Biomedical and NeuroMotor Sciences (DIBINEM), University of Bologna, Italy; 2: IRCCS Istituto delle Scienze Neurologiche di Bologna, Programma di Neurogenetica, Bologna, Italy; 3: Dept. Pharmacy and Biotechnology (FABIT), University of Bologna, Italy; 4: Dept. Chemistry, Life Science and Environmental Sustainability, University of Parma, Italy Mitochondria hormesis delays aging and associated diseases in C. elegans impacting on key ferroptosis players 1: Leibniz Research Institute for Environmental Medicine (IUF), Düsseldorf, Germany; 2: Humboldt-Universität zu Berlin, Berlin, Germany; 3: Institute of Clinical Medicine, Department of Clinical Molecular Biology, University of Oslo, Norway; 4: Institute of Clinical Chemistry and Laboratory Diagnostic, Medical Faculty, Heinrich Heine University of Düsseldorf, Germany Cross-talk between mitochondria and immunoproteasomes upon mitochondrial dysfunction IMol Polish Academy of Sciences, Warsaw, Poland Diagnostic examination of kinase inhibitors by bioenergetic profiling of cancer cell models reveals off-target drug effects 1: Division of Medical Biochemistry, Medical University of Innsbruck, Innrain 80/82, 6020 Innsbruck, Austria; 2: Tyrolean Cancer Research Institute (TKFI), Innrain 66, 6020 Innsbruck, Austria.; 3: Institute of Biochemistry and Center for Molecular Biosciences, University of Innsbruck, Innrain 80/82, 6020 Innsbruck, Austria; 4: Oroboros Instruments, Schoepfstrasse 18, 6020 Innsbruck, Austria Leukemia cells undergo metabolic remodeling and become vulnerable to mitochondrial translation inhibition University of Miami, United States of America Metabolic reprogramming of bone-marrow mesenchymal stem cells leads to impaired bone formation in m.3243A>G carriers 1: Dept. of Endocrinology, Odense University Hospital (OUH), Odense, Denmark; 2: The Molecular Endocrinology & Stem Cell Research Unit (KMEB), Molecular Endocrinology, University of Southern (SDU), Denmark; 3: Dept. of Molecular Diagnostics, Aalborg University Hospital, Aalborg; 4: Department of Biomedicine, Aarhus University, Aarhus, Denmark; 5: Khondrion BV, Nijmegen, The Netherlands; 6: Radboud Center for Mitochondrial Medicine, Radboud University Medical Center, Nijmegen, The Netherlands; 7: Dept. of Neurology, Rigshospitalet, Copenhagen, Denmark; 8: Dept. of Endocrinology, Hospital of Southwest, Esbjerg, Denmark; 9: Dept. of Clinical Research, SDU, Denmark; 10: Clinical Cell Biology, Dept. of Pathology, OUH, Denmark; 11: Dept. of Molecular Medicine, SDU, Denmark; 12: Dept. of Forensic Medicine, AU, Denmark; 13: Steno Diabetes Centre Odense, OUH, Denmark; 14: Dept. of Clinical Genetics, Aalborg University Hospital, Denmark Nucleus Associated Mitochondria (NAM) drive a cholesterol-mediated mechanism of Temozolomide resistance in glioblastoma cells 1: Department of Biology, University of Rome Tor Vergata, 00133, Rome, Italy; 2: Department of Biophysics, and Centre of Biotechnology, Universida de Federal do Rio Grande do Sul (UFRGS), Porto Alegre, RS, Brazil; 3: Department of Clinical and Molecular Medicine, University of Rome La Sapienza, 00198 Rome, Italy; 4: Department of Comparative Biomedical Sciences, The Royal Veterinary College, University of London; 5: Department of Biochemistry, Universidade Federal do Rio Grandedo Sul (UFRGS), Porto Alegre, RS, Brazil; 6: Department of Neurosurgery, Manchester Academic Health Science Centre, Northern Care Alliance, Salford UK; 7: Department of Cellular Pathology, Northern Care Alliance, Salford UK; 8: Laboratory of Electron Microscopy, Department of Epidemiology and Preclinical Research National Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, Rome, Italy; 9: Geoffrey Jefferson Brain Research Centre, Division of Neuroscience, School of Biological Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, UK; 10: UCL Consortium for Mitochondrial Research, University College London, WC1 6BT, London, UK; 11: Experimental Research Center, Hospital de Clínicas de Porto Alegre, Porto Alegre 90035-903, Rio Grande do Sul, Brazil Upregulation of COX4-2 via HIF-1α and replicative stress and impaired nuclear DNA damage response in mitochondrial COX4-1 deficiency Hadassah Medical Center and Hebrew University of Jerusalem, Israel Analysis of mitochondrial function using novel detection reagents 1: DOJINDO LABORATORIES; 2: Gunma University Mitochondrial dynamics in cancer cells: relationship between the F1Fo-ATPase inhibitor IF1 and the mitochondrial the fusion-fission machinery Department of Biomedical and Neuromotor Sciences, University of Bologna Melatonin overcomes resistance to CDDP treatment associated with the overexpression of the ATP-driven transmembrane efflux pumps 1: Institute of Biotechnology; 2: Biomedical Research Centre; 3: University of Granada, Spain Therapeutic capacity of exercise and melatonin against inflammation and mitochondrial dysfunction in the iMS-Bmal1-/- model of sarcopenia. 1: Departamento de Fisiología, Facultad de Medicina, Centro de Investigación Biomédica (CIBM), Universidad de Granada, Granada, Spain.; 2: Instituto de Investigación Biosanitaria de Granada (Ibs.Granada), Granada, Spain.; 3: Centro de Investigación Biomédica en Red de Fragilidad y Envejecimiento Saludable (CIBERfes), Madrid, Spain. Astrocytic CREB neuroprotection in experimental traumatic brain injury is associated with regulation of energetics and lipid metabolism: role of lactate 1: Universitat Autònoma de Barcelona, Institut de Neurociències, Bellaterra, Spain; 2: Neurocentre Magendie, Inserm U1215, Bordeaux, France; 3: Universitat de Lleida, Institut de Recerca Biomèdica, Lleida, Spain; 4: Georgia Institute of Technology, Georgia, United States of America; 5: Beatson Institute for Cancer Research, Glasgow, United Kingdom; 6: ICREA, Barcelona, Spain ROS induced mitochondrial hormesis partially protects from SGAs mitochondrial toxicity and cardiovascular disease. 1: Instituto de Investigaciones Biomédicas Alberto Sols, Spain; 2: Universidad de Valencia; 3: Instituto de Investigación Sanitaria La Princesa; 4: CBMSO; 5: Universidad Autónoma de Madrid Mitochondrial metabolism in breast cancer and cancer-associated adipose tissue 1: Institute for Biological Research "Sinisa Stankovic"- National Institute of Republic of Serbia, University of Belgrade, Serbia; 2: Faculty of Medicine, University of Novi Sad, Novi Sad, Serbia; 3: Faculty of Biology, University of Belgrade, Belgrade, Serbia Reorganization of the energy metabolism: from colon polyps to colorectal cancer 1: National Institute of Chemical Physics and Biophysics, Estonia; 2: North Estonia Medical Centre, Oncology and Haematology Clinic, Tallinn, Estonia Role of NcoR1 and PGC-1 for mitochondrial dysfunction in skeletal muscle of ovariectomized mice Korea Food Research Institute, Korea, Republic of (South Korea) Melatonin drives apoptosis in head and neck cancer by increasing mitochondrial ROS generated via reverse electron transport 1: Institute of Biotechnology, Biomedical Research Center, Health Sciences Technology Park, University of Granada, Granada, Spain; 2: Department of Physiology, Faculty of Medicine, University of Granada, Granada, Spain; 3: Centro de Investigación Biomédica en Red Fragilidad y Envejecimiento Saludable (CIBERFES), Instituto de Investigación Biosanitaria (Ibs), Granada, San Cecilio University Hospital, Granada, Spain Differences in life expectancy of rats with inherited high and low exercise capacity correlate with mitochondrial function in skeletal muscle 1: University Hospital of Friedrich-Schiller-University Jena, Germany; 2: The University of Toledo, Toledo, OH; 3: University of Michigan, Ann Arbor, MI Modulation of the activity of human mitochondrial protease complex ClpXP as potential therapeutic strategy for cancer University of Bari "Aldo Moro", Italy Mitochondrial respiratory function in peripheral blood cells across the human life span 1: Lund University, Department of Clinical Sciences Lund, Mitochondrial Medicine, Lund, Sweden; 2: Lund University, Skåne University Hospital, Department of Clinical Sciences Lund, Otorhinolaryngology, Head and Neck Surgery, Lund, Sweden; 3: A&E Department, Kungälv Hospital, Kungälv, Sweden; 4: Department of Neurosurgery, Rigshospitalet, Copenhagen, Denmark; 5: Lund University, Department of Clinical Sciences Lund, Translational Neurology Group and Wallenberg Center for Molecular Medicine, Lund, Sweden; 6: Skåne University Hospital, Department of Intensive- and perioperative Care, Malmö, Sweden Diagnostic value of urine organic acid analysis for primary mitochondrial disorders Research Centre for Medical Genetics, Russian Federation Exercise and melatonin counteract Bmal1 loss-dependent sarcopenia in mouse skeletal muscle by improving mitochondrial ultrastructure and function 1: Departamento de Fisiología, Facultad de Medicina, Centro de Investigación Biomédica (CIBM), Universidad de Granada, Granada, Spain.; 2: Instituto de Investigación Biosanitaria de Granada (Ibs.Granada), Granada, Spain.; 3: Centro de Investigación Biomédica en Red de Fragilidad y Envejecimiento Saludable (CIBERfes), Madrid, Spain. Uncovering the OXPHOS complexes' interdependence mechanism 1: Laboratory of Bioenergetics, Institute of Physiology, Czech Academy of Sciences, Czech Republic; 2: Laboratory of Molecular Therapy of Cancer, Institute of Biotechnology, Czech Academy of Sciences, Vestec, Czech Republic Challenging the norm – outcome measure selection for evaluating therapeutic response in patients with Primary Mitochondrial Myopathy after 12 weeks of treatment with REN001, a novel PPARδ agonist. 1: Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, UK; 2: National Institute for Health and Care Research (NIHR) Newcastle Biomedical Research Centre (BRC), Newcastle University and The Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK; 3: Wellcome Centre for Mitochondrial Research, Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, UK; 4: NHS Highly Specialised Service for Rare Mitochondrial Disorders, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK; 5: The Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK; 6: Department of Neuromuscular Diseases, UCL Queen Square Institute of Neurology and The National Hospital for Neurology and Neurosurgery, London, UK; 7: NHS Highly Specialised Service for Rare Mitochondrial Disorders, Queen Square Centre for Neuromuscular Diseases, The National Hospital for Neurology and Neurosurgery, London, UK Indirect comparison of lenadogene nolparvovec gene therapy versus natural history in m.11778G>A MT-ND4 Leber hereditary optic neuropathy patients 1: Departments of Ophthalmology, Neurology and Neurological Surgery, Emory University School of Medicine, Atlanta, GA, USA; 2: Departments of Neurology and Ophthalmology, Wills Eye Hospital and Thomas Jefferson University, Philadelphia, PA, USA; 3: IRCCS Istituto delle Scienze Neurologiche di Bologna, Programma di Neurogenetica, Bologna, Italy; 4: Cambridge Centre for Brain Repair and MRC Mitochondrial Biology Unit, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK; 5: Sue Anschutz-Rodgers University of Colorado Eye Center, University of Colorado School of Medicine, Aurora, CO, USA; 6: Department of Neuro Ophthalmology and Emergencies, Rothschild Foundation Hospital, Paris, France; 7: Department of Ophthalmology, Taipei Veterans General Hospital, National Yang Ming Chiao Tung University, Taipei, Taiwan; 8: Department of Ophthalmology, Neurology, and Pediatrics, Vanderbilt University, and Vanderbilt Eye Institute, Vanderbilt University Medical Center, Nashville, TN, USA; 9: Department of Ophthalmology and Center for Medical Genetics, Ghent University Hospital, and Department of Head & Skin, Ghent University, Ghent, Belgium; 10: Department of Neurology, Friedrich-Baur-Institute, University Hospital, Ludwig-Maximilians-University Munich, Munich, Germany; 11: Doheny Eye Institute, UCLA School of Medicine, Los Angeles, CA, USA; 12: Department of Ophthalmology, Alcala University, Madrid, Spain; 13: Department of Ophthalmology, Massachusetts Eye & Ear, Harvard Medical School, Boston, MA, USA; 14: Department of Ophthalmology, Icahn School of Medicine at Mount Sinai, New York, NY, USA; 15: GenSight Biologics, Paris, France; 16: Sorbonne Université, INSERM, CNRS, Institut de la Vision, Paris, France The mitochondrial stress, brain imaging, and epigenetics study (MiSBIE) 1: Columbia University Irving Medical Center, United States of America; 2: Université de Montréal, Canada; 3: Université de Bordeaux, France; 4: Dartmouth College, Uniter States of America Free cytosolic-mitochondrial DNA triggers a potent type-I Interferon response in Kearns–Sayre patients counteracted by mofetil mycophenolate 1: Unit of Cellular Biology and Diagnosis of Mitochondrial Diseases, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy; 2: Division of Rheumatology, Bambino Gesù Children’s Hospital, IRCCS, Rome, Italy; 3: Division of Metabolism, Bambino Gesù Children’s Hospital, IRCCS, Rome, Italy; 4: Research Unit of Muscular and Neurodegenerative Disorders, Bambino Gesù Children’s Hospital, IRCCS, Rome, Italy Fumarate induces mtDNA release via mitochondrial-derived vesicles and drives innate immunity 1: Medical Research Council, MBU,University of Cambridge, UK; 2: Medical Research Council Cancer Unit,University of Cambridge, UK; 3: CECAD Research Centre, University of Cologne, Cologne, Germany Impaired inflammatory response to lipopolysaccharide in fibroblasts from patients with long-chain fatty acid oxidation disorders 1: Laboratory Genetic Metabolic Diseases, Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands; 2: Research Unit for Molecular Medicine, Department of Clinical Medicine, Aarhus University and Aarhus University Hospital, Aarhus, Denmark; 3: Department of Biomedicine, Aarhus Research Center for Innate Immunology, Aarhus University, Aarhus, Denmark; 4: Department of Experimental Vascular Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands; 5: Core Facility Metabolomics, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, The Netherlands Functional characterisation of the human mitochondrial disaggregase, CLPB 1: Department of Biochemistry and Pharmacology, The Bio21 Molecular Science and Biotechnology Institute, The University of Melbourne, Parkville VIC 3010, Australia; 2: Murdoch Children’s Research Institute, Royal Children’s Hospital and Department of Paediatrics, The University of Melbourne, Parkville VIC 3052, Australia; 3: Victorian Clinical Genetics Services, Royal Children’s Hospital, Melbourne, Parkville VIC 3052, Australia High fat diet ameliorates the mitochondrial cardiomyopathy of CHCHD10 mutant mice Weill Cornell Medicine, United States of America The mitochondrial inhibitor IF1 has a dual role in cancer 1: Department of Biomedical and Neuromotor Sciences, University of Bologna; 2: Department of Chemical Science, University of Padova; 3: Department of Biology, University of Padova, Padova Tractography of the anterior optic pathway provides biomarkers of pathological change in Leber’s Hereditary Optic Neuropathy 1: Department of Biomedical and Neuromotor Sciences, University of Bologna, Italy; 2: IRCCS Instituto delle Scienze Neurologiche di Bologna, Bologna, Italy; 3: Department of Physics and Astronomy, University of Bologna, Italy; 4: Department of Life Quality Studies, University of Bologna A novel role of Keap1/PGAM5 complex: ROS sensor for inducing mitophagy 1: University of Tartu, Estonia; 2: University Paris-Saclay, INSERM UMR-S, France |
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4:30pm - 6:00pm |
Session 3.4: Clinical 2: natural history, biomarkers and outcome measures Location: Bologna Congress Center - Sala Europa Chair: Costanza Lamperti Chair: Alessandra Maresca Optimising interventional trials: how natural history studies and digital technologies can drive innovation 1: Wellcome Centre for Mitochondrial Research, Newcastle University, Newcastle upon Tyne, United Kingdom; 2: University of Pisa, Italy Invited Identifying circulating biomarkers to monitor mitochondrial disease severity Massachusetts General Hospital, United States of America Oral presentation National mitochondrial disease registry in England: linking genetics with routinely collected healthcare data 1: Department of Clinical Neurosciences, School of Clinical Medicine, University of Cambridge, Cambridge, UK; 2: Medical Research Council Mitochondrial Biology Unit, University of Cambridge, Cambridge, UK; 3: National Disease Registration Service, NHS Digital, Leeds, UK; 4: Department of Neuromuscular Diseases, UCL Queen Square Institute of Neurology and The National Hospital for Neurology and Neurosurgery, London, UK; 5: NHS Highly Specialised Services for Rare Mitochondrial Disorders – Oxford Centre, Oxford University Hospitals NHS Foundation Trust, Oxford, UK Oral presentation Status epilepticus in POLG disease 1: Department of Paediatrics and Adolescent Medicine, Haukeland University Hospital, Norway; 2: Department of Clinical Medicine (K1), University of Bergen, Norway; 3: Centre for Inherited Metabolic Diseases, Karolinska University Hospital, Stockholm, Sweden; 4: Department of Neuropediatrics, Astrid Lindgren Childrens Hospital, Karolinska University Hospital, Stockholm, Sweden; 5: Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden; 6: Department of Paediatric and Adolescent Medicine, University Hospital of North Norway, Tromso, Norway; 7: Paediatric Research Group, Department of Clinical Medicine, UiT- The Arctic University of Norway, Tromso, Norway; 8: Women and Children's Division, Department of Clinical Neurosciences for Children, Oslo University Hospital, Oslo, Norway and Unit for Congenital and Hereditary Neuromuscular Disorders, Department of Neurology, Oslo University Hospital, Oslo, Norway; 9: Department of Neurology, Oslo University Hospital, Oslo, Norway; 10: Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway; 11: Department of Neuroscience and Movement Science, Norwegian University of Science and Technology, Trondheim, Norway; 12: Department of Neurology and Clinical Neurophysiology, St. Olav's University Hospital, Trondheim, Norway; 13: Department of Clinical Genetics, Copenhagen University Hospital Rigshospitalet, Copenhagen, Denmark; 14: Facultiy of Health, Medicine and Life Sciences, Department of Toxicology, , University of Maastricht, Maastricht, The Netherlands; 15: Neurometabolic Disorders Unit, Department of Child Neurology/ Department of Genetics and Molecular Medicine, Sant Joan de Déu Children´s Hospital, Barcelona, Spain; 16: Department of Pediatric Neurology, Children's Hospital and Pediatric Research Center, University of Helsinki and Helsinki University Hospital, Helsinki, Finland; 17: Stem Cells and Metabolism Research Program, Faculty of Medicine, University of Helsinki, Helsinki, Finland.; 18: Research Unit of Clinical Medicine, University of Oulu, Oulu, Finland; 19: Department of Pediatric Neurology, Clinic for Children and Adolescents and Medical Research Center, Oulu University Hospital, Oulu, Finland; 20: Research Unit of Clinical Medicine, Neurology, and Medical Research Center Oulu, Oulu University hospital and university of Oulu, Oulu Finland; 21: Neurocenter , Oulu University Hospital ,Oulu Finland; 22: Movement Disorders Unit, Institut de Recerca Sant Joan de Déu, CIBERER-ISCIII, Barcelona, Spain; 23: European Reference Network for Rare Neurological Diseases (ERN-RND), Barcelona, Spain; 24: Norwegian national Unit for Newborn Screening, Division of Pediatric and adolescent Medicine, Oslo University Hospital, Oslo, Norway; 25: European Reference Network for Hereditary Metabolic Disorder; 26: Department of Medical Genetics, Haukeland University Hospital, Bergen, Norway; 27: Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK; 28: Department of Pediatrics, Institute of Clinical Sciences, University of Gothenburg, Queen Silvia Children's Hospital, Sahlgrenska University Hospital, Gothenburg, Sweden; 29: Mitochondrial Research Group, UCL Great Ormond Street Institute of Child Health, London, UK; 30: Metabolic Unit, Great Ormond Street Hospital for Children NHS Foundation Trust, London, UK; 31: Department of Neurology, Haukeland University Hospital, 5021 Bergen, Norway Flash Talk Challenging the norm – outcome measure selection for evaluating therapeutic response in patients with Primary Mitochondrial Myopathy after 12 weeks of treatment with REN001, a novel PPARδ agonist. 1: Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, UK; 2: National Institute for Health and Care Research (NIHR) Newcastle Biomedical Research Centre (BRC), Newcastle University and The Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK; 3: Wellcome Centre for Mitochondrial Research, Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, UK; 4: NHS Highly Specialised Service for Rare Mitochondrial Disorders, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK; 5: The Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK; 6: Department of Neuromuscular Diseases, UCL Queen Square Institute of Neurology and The National Hospital for Neurology and Neurosurgery, London, UK; 7: NHS Highly Specialised Service for Rare Mitochondrial Disorders, Queen Square Centre for Neuromuscular Diseases, The National Hospital for Neurology and Neurosurgery, London, UK Flash Talk Indirect comparison of lenadogene nolparvovec gene therapy versus natural history in m.11778G>A MT-ND4 Leber hereditary optic neuropathy patients 1: Departments of Ophthalmology, Neurology and Neurological Surgery, Emory University School of Medicine, Atlanta, GA, USA; 2: Departments of Neurology and Ophthalmology, Wills Eye Hospital and Thomas Jefferson University, Philadelphia, PA, USA; 3: IRCCS Istituto delle Scienze Neurologiche di Bologna, Programma di Neurogenetica, Bologna, Italy; 4: Cambridge Centre for Brain Repair and MRC Mitochondrial Biology Unit, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK; 5: Sue Anschutz-Rodgers University of Colorado Eye Center, University of Colorado School of Medicine, Aurora, CO, USA; 6: Department of Neuro Ophthalmology and Emergencies, Rothschild Foundation Hospital, Paris, France; 7: Department of Ophthalmology, Taipei Veterans General Hospital, National Yang Ming Chiao Tung University, Taipei, Taiwan; 8: Department of Ophthalmology, Neurology, and Pediatrics, Vanderbilt University, and Vanderbilt Eye Institute, Vanderbilt University Medical Center, Nashville, TN, USA; 9: Department of Ophthalmology and Center for Medical Genetics, Ghent University Hospital, and Department of Head & Skin, Ghent University, Ghent, Belgium; 10: Department of Neurology, Friedrich-Baur-Institute, University Hospital, Ludwig-Maximilians-University Munich, Munich, Germany; 11: Doheny Eye Institute, UCLA School of Medicine, Los Angeles, CA, USA; 12: Department of Ophthalmology, Alcala University, Madrid, Spain; 13: Department of Ophthalmology, Massachusetts Eye & Ear, Harvard Medical School, Boston, MA, USA; 14: Department of Ophthalmology, Icahn School of Medicine at Mount Sinai, New York, NY, USA; 15: GenSight Biologics, Paris, France; 16: Sorbonne Université, INSERM, CNRS, Institut de la Vision, Paris, France Flash Talk The mitochondrial stress, brain imaging, and epigenetics study (MiSBIE) 1: Columbia University Irving Medical Center, United States of America; 2: Université de Montréal, Canada; 3: Université de Bordeaux, France; 4: Dartmouth College, Uniter States of America |
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6:00pm - 7:00pm |
Poster session Location: Bologna Congress Center Session topics:
- Mitochondrial mechanisms in neurodegeneration and neurodevelopment - The impact of mtDNA variation and environment on rare and common diseases SARM1 deletion delays cerebellar but not spinal cord degeneration in an enhanced mouse model of SPG7 deficiency 1: Institute for Genetics, University of Cologne, Cologne 50931, Germany; 2: Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Cologne 50931, Germany; 3: Max Planck Institute for Biology of Ageing, Cologne 50931, Germany; 4: Center for Molecular Medicine (CMMC), University of Cologne, Cologne 50931, Germany Pathobiology of cerebellar degeneration in the Harlequin mouse, a proteomic and system biology approach 1: Mitochondrial and Neuromuscular Diseases Laboratory, Instituto de Investigación Sanitaria Hospital ‘12 de Octubre’ (‘imas12’), Madrid, Spain; 2: Spanish Network for Biomedical Research in Rare Diseases (CIBERER), U723, Spain.; 3: Servicio de Bioquímica Clínica. Hospital Universitario ‘12 de Octubre’. Madrid, Spain; 4: Servicio de Genética. Hospital Universitario ‘12 de Octubre’. Madrid, Spain; 5: Faculty of Sports Sciences, European University of Madrid, Madrid, Spain; 6: Spanish Network for Biomedical Research in Fragility and Healthy Aging (CIBERFES), Madrid, Spain The role of mitochondrial transcriptional processes in the aetiology of Parkinson’s disease 1: Department of Medical and Molecular Genetics, School of Basic and Medical Biosciences, King’s College London, London, United Kingdom; 2: Department of Genetics and Genomic Medicine Research & Teaching, UCL GOS Institute of Child Health, London, WC1N 1EH, UK; 3: Department of Neurodegenerative Disease, Queen Square Institute of Neurology, UCL, London WC1N 3BG, UK; 4: NIHR Great Ormond Street Hospital Biomedical Research Centre, University College London, London, WC1N 1EH, UK; 5: Department of Information and Communications Engineering Faculty of Informatics, Espinardo Campus, University of Murcia, Murcia, 30100, Spain Towards a unitary hypothesis of Alzheimer disease pathogenesis 1: Columbia University, USA; 2: Centro de Investigaciones Biológicas “Margarita Salas”, Madrid, Spain An experimental protocol for in vivo imaging of brain mitochondrial properties with multiphoton microscopy Instituto de Medicina Molecular João Lobo Antunes, Faculdade de Medicina, Universidade de Lisboa, 1649-028 Lisbon, Portugal Exploiting hiPSCs-derived astrocytes from CoPAN patients as cell model to study iron accumulation. 1: San Raffaele Scientific Institute; 2: Vita-Salute San Raffaele, Italy; 3: Fondazione IRCCS Istituto Neurologico Carlo Besta; 4: Institute of Neuroscience National Research Council Secondary mitochondrial impairment in muscle of pediatric patients unrelated to the genes diagnosed by WES: are these mitochondrial diseases? 1: IRCCS Istituto delle Scienze Neurologiche di Bologna, Programma di Neurogenetica, Bologna, Italy; 2: Department of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy; 3: IRCCS Istituto delle Scienze Neurologiche di Bologna, UOC di Neuropsichiatria dell'Età Pediatrica, Bologna, Italy; 4: Child Neuropsychiatry Unit, Department of Surgical Sciences, Dentistry, Gynecology and Pediatrics, University of Verona, Verona, Italy; 5: Department of Medical and Surgical Sciences, University of Bologna, Bologna, Italy; 6: Medical Genetics Unit, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy In vitro 2D and 3D neuronal model generation of MERRF disease to test therapeutic strategies 1: IRCCS Istituto delle Scienze Neurologiche di Bologna, Programma di Neurogenetica, Bologna, Italy; 2: Department of Biomedical and Neuromotor Sciences (DIBINEM), University of Bologna, Bologna, Italy; 3: Department of Radiological, Oncological and Pathological Sciences, Sapienza, University of Rome, Rome, Italy; 4: Department of General Pediatrics, Neonatology and Pediatric Cardiology, Medical Faculty, Heinrich Heine University, Düsseldorf, Germany Molecular mechanism of human mitochondrial chaperonin and its mutation in neurodegenerative disease Indiana University, United States of America Nucleus-associated mitochondria (NAM) control neuronal Ca2+ signalling and gene expression 1: University of Hertfordshire, Department of Clinical, Pharmaceutical and Biological Science, Hatfield, United Kingdom; 2: Discovery Research MRL UK, MSD, LBIC, London, United Kingdom; 3: William Harvey Research Institute, Queen Mary University of London, London, United Kingdom; 4: Proteomics Facility, Centre of Excellence for Mass Spectrometry, King’s College London, London, United Kingdom; 5: University of Padua, Department of Biomedical Sciences, Padua, Italy Autophagy controls the pathogenicity of OPA1 mutations in ADOA plus 1: Department of Translational Biomedicine and Neuroscience (DiBraiN), University of Bari Aldo Moro, Bari, Italy; 2: Molecular Medicine for Neurodegenerative and Neuromuscular Diseases Unit, IRCCS Fondazione Stella Maris, Pisa, Italy Investigating the function of CHCHD2-CHCHD10 complexes in mitochondria 1: Feil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY, USA; 2: Department of Neurology, Columbia University Medical Center, New York, NY, USA Sildenafil restores normal MMP in MILS-NPCs with impaired Complex V assembly and activity 1: University of Verona, Italy; 2: Department of General Pediatrics, Neonatology and Pediatric Cardiology, Duesseldorf University Hospital, Medical Faculty, Heinrich Heine University, Duesseldorf, Germany; 3: Charité-Universitätsmedizin Berlin, Department of Neuropediatrics, Berlin, Germany; 4: Unit of Medical Genetics and Neurogenetics, Fondazione IRCCS Istituto Neurologico "C.Besta", Milan, Italy; 5: Mitochondrial Medicine Laboratory, Department of Medical Biotechnology and Translational Medicine, University of Milan, Milan, Italy; 6: Max Delbrueck Center for Molecular Medicine (MDC), 13125 Berlin, Germany Mitochondrial dysfunction due to mRNA transport defects as a mechanism of neurodegeneration? Unraveling the role of TBCK in a human neuronal model 1: Center for Mitochondrial and Epigenomic Medicine, Children's Hospital of Philadelphia; 2: Division of Neurology, The Children's Hospital of Philadelphia Modelling COASY protein-associated neurodegeneration (CoPAN) in mice IRCCS Istituto Neurologico C. Besta, Italy Neural stem cell niche-interactions in mitochondrial disease University of Cambridge, United Kingdom Mutant SPART causes defects in mitochondrial protein import and bioenergetics reversed by Coenzyme Q 1: Department of Medical and Surgical Sciences, University of Bologna, Bologna, Italy, 40138; 2: U.O. Genetica Medica, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy, 40138; 3: Center for Applied Biomedical Research (CRBA), University of Bologna, Bologna, Italy, 40138; 4: Department of Pharmacy and Biotechnology, University of Bologna, Bologna, Italy, 40126; 5: Institut für Humangenetik, Universitätsklinikum Essen, Universität Duisburg-Essen, Essen, Germany, 45122; 6: Department of Veterinary Sciences, University of Bologna, Bologna, Italy, 40064; 7: Institute of Medical Genetics and Applied Genomics, University of Tübingen, Tübingen, Germany, 72076; 8: Center for Rare Diseases, University of Tübingen, Tübingen, Germany, 72076; 9: Department of Pediatric Neurology, Centre for Neuromuscular Disorders, Centre for Translational Neuro- and Behavioral Sciences, University Duisburg-Essen, Essen, Germany, 45122 Characterization of a novel brain-specific mouse model of Leigh Syndrome Neuroscience Institute-Autonomous University of Barcelona, Spain Investigating FA physiopathology in human iPSC-derived DRG organoïds 1: Institut NeuroMyoGene, PGNM UMR5261, INSERM U1315, Université Claude Bernard Lyon I Faculté de médecine Rockefeller, Lyon 08 France; 2: UT Southwestern Medical Center, 5323 Harry Hines Blvd. Suite NL.9.108 TX75390-8813 Dallas USA A novel TUBB2A variant associated with pediatric neurodegeneration links microtubule stability to mitochondrial function 1: Center for Mitochondrial and Epigenomic Medicine, The Children’s Hospital of Philadelphia; 2: Division of Neurology, Department of Pediatrics, The Children's Hospital of Philadelphia; 3: Department of Radiology, The Children’s Hospital of Philadelphia; 4: Department of Pathology and Cell Biology, Columbia University Characterization and functional analysis of a zebrafish knockdown of the mitochondrial DNA replication gene ssbp1 1: Institute for Neurosciences of Montpellier (INM) U1298, France; 2: Molecular Mechanisms in Neurodegenerative Dementia (MMDN) U1198, France Deep mitochondrial genotyping reveals altered mitochondrial quality control mechanisms in advanced cellular models of Parkinson’s disease Institute for Biomedicine, Eurac Research, Affiliated Institute of the University of Lübeck, Bolzano, Italy Defining the nuclear genetic architecture of a maternally-inherited mitochondrial disorder 1: Wellcome Centre for Mitochondrial Research and Institute for Translational and Clinical Research, ewcastle University, United Kingdom; 2: NHS Highly Specialised Mitochondrial Diagnostic Laboratory, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK; 3: Department of Neurology, Friedrich-Baur-Institute, University Hospital of the Ludwig-Maximilians-University (LMU Klinikum), Munich, Germany; 4: Department of Neuromuscular Diseases, UCL Queen Square Institute of Neurology and The National Hospital for Neurology and Neurosurgery, London, UK; 5: Exeter Genomics Laboratory, Royal Devon and Exeter NHS Foundation Trust, Exeter, UK; 6: Institute of Biomedical and Clinical Science, University of Exeter Medical School, Exeter, UK; 7: Munich Cluster for Systems Neurology (SyNergy), Munich, Germany; 8: German Center for Neurodegenerative Diseases (DZNE), Munich, Germany; 9: Department of Neurology, University Hospital Bonn, Bonn, Germany; 10: Neurological Institute of Pisa, Italy; 11: Institute of Human Genetics, School of Medicine, Technische Universität München, München, Germany; 12: Institute of Neurogenomics, Helmholtz Zentrum München - German Research Center for Environmental Health, Neuherberg, Germany; 13: Department of Neurology, Universitätsklinikum Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany; 14: Department of Neurology, Martin-Luther-University Halle-Wittenberg, 06120 Halle (Saale), Germany; 15: Neurogenetics Unit, The National Hospital for Neurology and Neurosurgery, London, UK; 16: Population Health Sciences Institute, Newcastle University, UK OPA3 loss causes alterations in mitocondrial dynamics and autophagy processes 1: IRCCS Istituto delle Scienze Neurologiche di Bologna, Programma di Neurogenetica, via Altura 3, 40139, Bologna, Italy; 2: Department of Biomedical and NeuroMotor Sciences, University of Bologna, via Altura 3, 40139, Bologna, Italy Mitochondrial fusion- and transport-specific roles in neuronal dysfunction 1: Institute for Biochemistry, University of Cologne, Cologne, Germany; 2: Cologne Excellence Cluster on Cellular Stress Response in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany ER-Mitochondria are affected during ageing in enteric neurons Inserm U1235, France Identification of dysregulated molecular pathways in Frataxin deficient Proprioceptive Neurons INMG-PGNM, France Mitochondrial dysfunction in dorsal root ganglia in Friedreich ataxia mouse and cell models: role of SirT3 Dept. Ciències Mèdiques Bàsiques, Fac. Medicina, Universitat de Lleida. IRBLleida. Lleida (Spain). MPTP-induced parkinsonism in zebrafish provokes chronodisruption-related loss of daily melatonin and locomotor activity rhythms and mitochondrial dynamics shift, which are restored by melatonin treatment 1: Departamento de Fisiología, Facultad de Medicina, Centro de Investigación Biomédica (CIBM), Universidad de Granada, Granada, Spain.; 2: Instituto de Investigación Biosanitaria de Granada (Ibs.Granada), Granada, Spain.; 3: Centro de Investigación Biomédica en Red de Fragilidad y Envejecimiento Saludable (CIBERfes), Madrid, Spain. Activation of integrated mitochondrial stress response in PRKN Parkinson Disease 1: Inherited metabolic diseases and muscular disorders Lab, Cellex - Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Faculty of Medicine and Health Science - University of Barcelona (UB), Department of Internal Medicine - Hospital Clínic of Barcelona (HCB), 08036 Barcelona, Spain, and Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER, U722), 28029 Madrid, Spain.; 2: Research Program of Stem Cells and Metabolism, Faculty of Medicine, University of Helsinki, Helsinki 00290, Finland; HUSlab, Helsinki University Hospital, Helsinki 00290, Finland;; 3: Laboratory of Parkinson Disease and Other Neurodegenerative Movement Disorders, IDIBAPS-Hospital Clínic de Barcelona, Institut de Neurociències, UB, 08036 Barcelona, Spain and Centre for Networked Biomedical Research on Neurodegenerative Diseases (CIBERNED CB06/05/0018), 28029 Madrid, Spain.; 4: Department of Clinical Biochemistry, Institut de Recerca de Sant Joan de Deu, Esplugues de Llobregat, 08036 Barcelona, Spain, and CIBERER, 28029 Madrid, Spain.; 5: Department of Statistics, Biology Faculty, UB, Barcelona, Spain; 6: Institute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology (BIST), 08028 Barcelona, Spain; Department of Biochemistry and Molecular Biomedicine, UB, E-08028 Barcelona, Spain; U731, CIBERER, 08028 Barcelona, Spain; Delineating the neurodegenerative mechanisms underpinning epilepsy in Alpers’ syndrome 1: Wellcome Centre for Mitochondrial Research, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, UK; 2: Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, UK; 3: NHS Highly Specialised Service for Rare Mitochondrial Disorders of Adults and Children, Newcastle Upon Tyne Hospitals NHS Foundation Trust, Newcastle Upon Tyne, UK Understanding the effects of hyperbaric oxygen therapy on Alzheimer’s disease mouse model Tel-Aviv University, Israel Analyzing the mitochondrial HPDL protein in fish and human models IRCCS Fondazione Stella Maris, Italy Modulation of mitophagy, mitochondrial and autophagy phenotypes in LRRK2 Parkinson’s patient fibroblast-derived dopaminergic neurons by small molecules 1: Sheffield Institute for Translational Neuroscience (SITraN), The University of Sheffield, Sheffield, UK.; 2: Verge Genomics, South San Francisco, CA, USA. Proinflammatory cytokines induce alterations of mitochondrial functions and dynamics in neurons Institute of Neuroscience, National Chengchi University, Taiwan Mitochondrial dysfunction is involved in progranulin-related frontotemporal dementia 1: Department of Neuromuscular Diseases, UCL Queen Square Institute of Neurology, London, UK; 2: Neurogenetics Unit, Rare and Inherited Disease Genomic Laboratory, North Thames Genomic Laboratory Hub, London, UK; 3: Dementia Research Centre, Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, London, UK; 4: Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, London, UK; 5: Department of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, Royal Free Campus, London, UK; 6: NHS Highly Specialised Service for Rare Mitochondrial Disorders, Queen Square Centre for Neuromuscular Diseases, The National Hospital for Neurology and Neurosurgery, London, UK Morphological characterization of the progression of mitochondrial encephalopathy associated with CoQ10 deficiency 1: Physiology Department, Biomedical Research Center, University of Granada, Granada, Spain; 2: Biofisika Institute (CSIC, UPV-EHU) and Department of Biochemistry and Molecular Biology, University of Basque Country, Leioa, Spain; 3: Ibs.Granada, Granada, Spain The vanishing dopamine in Parkinson’s disease IST Austria, Austria Effect of UPO04 depending on GAA triplet hyperexpansion in Friedreich’s ataxia disease. Universidad Pablo de Olavide, Spain New cell model for studying mitochondrial dysfunction in Fragile X-associated tremor/ataxia syndrome Department of Gene Expression, Institute of Molecular Biology and Biotechnology, Adam Mickiewicz University, Poznan, Poland Development of an in vitro platform for preclinical investigations on EPM1 1: University of Eastern Finland, Finland; 2: Kuopio University Hospital, Finalnd Metabolic rewiring in iPSCs-derived neuron progenitor cells of patients with mutations of mitochondrial SLC25A12/AGC1 carrier 1: Department of Biosciences Biotechnologies and Environment, University of Bari, Italy; 2: Department of Pharmacy and BioTechnology, University of Bologna, Italy; 3: Institute of Human Genetics, University Hospital, Leipzig, Germany; 4: Hematology and Cell Therapy Unit, IRCCS-Istituto Tumori "Giovanni Paolo II, Bari, Italy; 5: Children's Hospital of Philadelphia Research Institute, Philadelphia, USA; 6: University Children's Hospital, Heinrich-Heine-University, Düsseldorf, Germany Mitochondrial function at the neuromuscular junction in motor neuron disease 1: Wellcome Centre for Mitochondrial Research, Newcastle University, United Kingdom; 2: Department of Neuromuscular Disease, UCL Queen Square Institute of Neurology, Queen Square, London, UK; 3: The Francis Crick Institute, London, UK. A novel WDR45 variant in an encephalopathy mimicking Leigh syndrome with complex I deficiency 1: Child Neurology, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy.; 2: Department of Health Sciences,University of Milan, Milan, Italy; 3: Unit of Medical Genetics and Neurogenetics, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; 4: Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy Characterisation of mitochondrial dysfunction in Huntington’s disease patient-derived fibroblasts 1: University of Sheffield, Sheffield Institute for Translational Neuroscience, United Kingdom; 2: Nanna Therapeutics, Cambridge, UK Loss of mitochondrial chaperone Trap1 in mice causes changes in synaptic mitochondria function Centre of New Technologies, University of Warsaw, Poland Unveiling the metabolic signature of synaptic mitochondria Instituto de Medicina Molecular João Lobo Antunes, Portugal Aberration of mitochondrial ultrastructure in the skeletal muscle in patients with Parkinson’s disease 1: Neurocenter, Oulu University Hospital, Oulu, Finland; 2: Research Unit of Clinical Medicine, Medical Research Center, University of Oulu and Oulu University Hospital, Oulu Finland; 3: Electron microscopy, Biocenter Oulu, University of Oulu, Oulu, Finland; 4: Pathology, Turku University Hospital and University of Turku, Turku, Finland; 5: Pathology, Oulu University Hospital, Oulu, Finland; 6: Division of Orthopaedic and Trauma Surgery, Department of Surgery, Medical Research Center, University of Oulu and Oulu University Hospital, Oulu, Finland New insights into the pathogenicity of the MT-ATP6: m.9176T>C mutation by a patient cohort and transmitochondrial cybrids combined approach 1: Mitochondrial Diseases Laboratory, Research Institute, Universitary Hospital 12 de Octubre (Imas12), 28041 Madrid, Spain.; 2: Department of Pediatric Neurology, Hospital General Universitario de Toledo, Toledo, Spain.; 3: Biochemistry Department, Biomedical Research Institute 'Alberto Sols', CSIC, Faculty of Medicine, Autonomous University of Madrid, and Instituto de Investigación Sanitaria Hospital 12 de Octubre (Imas12), 28041 Madrid, Spain.; 4: iPS Cells Translational Research Group, Research Institute, Universitary Hospital 12 de Octubre (Imas12), 28041 Madrid, Spain.; 5: Centre for Biomedical Network Research on Rare Diseases (CIBERER), Spain. Determining the contribution of mitochondrial alterations to lung cancer in vivo Karolinska Institute, Sweden Gamma Peptide Nucleic Acids as a Mechanism for Targeting the Mitochondrial Genome 1: Department of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania, USA; 2: Department of Medicine, Vascular Medicine Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA; 3: Department of Chemistry and Center for Nucleic Acids Science and Technology, Carnegie Mellon University, Pittsburgh, Pennsylvania, USA; 4: Department of Chemistry, University of Massachusetts Amherst, Amherst, Massachusetts, USA Physiological variability in mitochondrial rRNA may predispose to metabolic syndrome 1: Laboratory of Bioenergetics, Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic; 2: Laboratory of Genetics of Model Diseases, Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic; 3: Laboratory of Translational Metabolism, Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic The European landscape of mitogenomes from LHON patients carrying the m.14484T>C/MT-ND6 pathogenic variant 1: University of Bologna, Italy; 2: University of Pavia, Pavia, Italy; 3: Laboratory of Bioinformatics, Fondazione IRCCS Casa Sollievo della Sofferenza, Rome, Italy; 4: IRCCS Institute of Neurological Sciences of Bologna, Bologna, Italy; 5: University of Tuebingen, Tuebingen, Germany; 6: Université LUNAM, Angers, France; 7: Universidad de Zaragoza, Zaragoza, Spain; 8: National Neurological Institute 'C. Besta', Milano, Italy; 9: Ludwig-Maximilians-Universität München, Munich, Germany; 10: UCLA, Los Angeles, California, USA; 11: University of Siena, Siena, Italy; 12: University of Newcastle, Newcastle upon Tyne, UK; 13: University of Cambridge, Cambridge, UK; 14: Moorfields Eye Hospital and UCL Institute of Ophthalmology, London, UK; 15: Erasmus Medical Centre, Rotterdam, The Netherlands; 16: PhD, Department of Biomedical and Neuromotor Sciences (DIBINEM), University of Bologna Mitochondrial DNA contribution to Parkinsonism: from mtDNA maintenance defects to primary mtDNA pathogenic variants 1: IRCCS Istituto delle Scienze Neurologiche, Italy; 2: Department of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy Combined fiber atrophy and impaired muscle regeneration capacity driven by mitochondrial DNA alterations underlie the development of sarcopenia 1: Department of Medical Laboratory Sciences, Masinde Muliro University of Science and Technology - Kakamega, Kenya; 2: Institute of Vegetative Physiology, University of Cologne - Cologne, Germany; 3: Max Planck Institute for Heart and Lung Research - Bad Nauheim, Germany; 4: Institute for Cardiovascular Physiology, University Medical Center - Göttingen, Germany; 5: Institute of Physiology I, Medical Faculty, University of Bonn - Bonn, Germany; 6: Center for Molecular Medicine Cologne - Cologne, Germany; 7: Cologne Excellence Cluster on Cellular Stress Responses in Aging-associated Diseases (CECAD) - Cologne, Germany; 8: University of Angers, UMR 6015 CNRS / 1083 INSERM, Mitovasc - Angers, France Examining the link between diet and metabolic risk score in individuals with bipolar disorder University of Toronto, Canada Mitochondrial morphology and function in mitochondrial disease 1: Newcastle University, United Kingdom; 2: Welcome Centre for Mitochondrial Research, Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, United Kingdom; 3: NHS Highly Specialised Service for Rare Mitochondrial Disorders, Newcastle upon Tyne, United Kingdom MtDNA sequence and copy number analysis of buffy coat DNA of primary open-angle glaucoma patients 1: University Eye Clinic Maastricht, Maastricht University Medical Center+, Maastricht, The Netherlands; 2: Department of Toxicogenomics, Maastricht University, Maastricht, The Netherlands; 3: School for Mental Health and Neuroscience, Maastricht University, Maastricht, The Netherlands; 4: Department of Clinical Genetics, Maastricht University Medical Center, Maastricht, The Netherlands; 5: Department of Dermatology, GROW-school for oncology and reproduction, Maastricht University Medical Center, Maastricht, The Netherlands MELAS syndrome pathophysiology in cellular models of the disease Universidad Pablo de Olavide, Spain Pathogenic mtDNA variants, in particular single large-scale mtDNA deletions, are strongly associated with post-lingual onset sensorineural hearing loss in primary mitochondrial disease 1: Otorhinolaryngology, Head and Neck Surgery, Department of Clinical Sciences Lund, Lund University, Skåne University Hospital, Sweden; 2: Mitochondrial Medicine Frontier Program, Division of Human Genetics, Department of Pediatrics, Children's Hospital of Philadelphia, USA; 3: Logopedics, Phoniatrics and Audiology, Department of Clinical Sciences Lund, Lund University, Sweden; 4: Department of Pediatrics, Perelman School of Medicine, University of Pennsylvania, USA; 5: Division of Biostatistics, Department of Pediatrics, Children's Hospital of Philadelphia, USA; 6: Mitochondrial Medicine, Department of Clinical Sciences Lund, Lund University, Sweden What can we learn from detrimental mitogenome mutations in cattle? 1: University of Zagreb - Faculty of Agriculture, 10000 Zagreb, Croatia; 2: University of Ljubljana - Veterinary Faculty, 1000 Ljubljana, Slovenia; 3: University of Ljubljana - Biotechnical Faculty, 1000 Ljubljana, Slovenia; 4: Croatian Veterinary Institute, 10000 Zagreb, Croatia; 5: Agricultural Institute of Slovenia, 1000 Ljubljana, Slovenia Mitochondrial DNA copy number measurements reveal systemic evidence for mitochondrial dysfunction in age-related macular degeneration 1: Medical University of Innsbruck, Austria; 2: University of Regensburg, Germany Multiple mitochondrial DNA deletions in patients with myopathy 1: Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA; 2: Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA Utilizing donor mitochondrial haplogroup as a potential screening tool for the risk of primary graft dysfunction 1: University of Toronto, Canada; 2: University Health Network, Toronto A rare variant m.4135T>C in the MT-ND1 gene leads to LHON and altered OXPHOS supercomplexes 1: Department of Pediatrics and Inherited Metabolic Disorders, Charles University, First Faculty of Medicine and General University Hospital in Prague, Prague, Czech Republic; 2: Department of Ophthalmology, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czech Republic; 3: Department of Biochemistry, Faculty of Science, Charles University, Prague, Czech Republic. Mitophagy is stalled in cultured fibroblasts harbouring Parkin mutations 1: Department of Women’s and Reproductive Health, University of Oxford, Oxford, UK.; 2: Inherited Movement Disorders Unit, Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, USA.; 3: Signalling Programme. The Babraham Institute, Cambridge, UK. Impact of mitochondrial DNA modifications in shaping personalized ETC complex activities 1: University of Oslo, Norway; 2: Oslo University Hospital Elucidating the role of ATF3 in the neuropathology of a mouse model of Leigh Syndrome 1: Institut de Neurociències, Universitat Autònoma de Barcelona. Bellaterra (Barcelona) 08193. Spain; 2: Department of Cell Biology, Physiology and Immunology, Universitat Autònoma de Barcelona. Bellaterra (Barcelona) 08193. Spain Deciphering the contribution of the Parvalbumin-expressing neurons in the motor, cognitive and social alterations in a mouse model of Leigh Syndrome 1: Autonomous University of Barcelona, Bellaterra, Spain; 2: Scripps Research, La Jolla, CA, USA CHCHD10 and SLP2 control the stability of the PHB complex : a key factor for motor neuron viability 1: Université Côte d’Azur, Inserm U1081, CNRS UMR7284, IRCAN, CHU de Nice, Nice (France); 2: Mitochondrial Biology Group, Institut Pasteur, CNRS UMR 3691, Paris (France); 3: Université Côte d’Azur, Centre Commun de Microscopie Appliquée, Nice (France); 4: Mécanismes Centraux et Périphériques de la Neurodégénérescence, Inserm U1118, UMR S1118, CRBS, Université de Strasbourg, Strasbourg (France) Mitochondrial dysfunction in peripheral blood mononuclear cells in different stages of Huntington´s disease 1: Department of Paediatrics and Inherited Metabolic Disorders, First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic; 2: Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic; 3: Department of Medical Biochemistry, University of Oslo and Oslo University Hospital, Oslo, Norway. The mitochondrial DNA depletion syndrome protein FBXL4 mediates the degradation of the mitophagy receptors BNIP3 and NIX to suppress mitophagy 1: School of Biomedical Sciences, Faculty of Medicine, University of Queensland, Brisbane, Australia; 2: Department of Biotechnology, School of Biotechnology, Viet Nam National University-International University, Ho Chi Minh City, Vietnam; 3: Department of Biochemistry and Molecular Pharmacology, New York University Grossman School of Medicine, New York, USA; 4: Perlmutter Cancer Center, New York University Grossman School of Medicine, New York, USA; 5: The University of Queensland, Institute for Molecular Bioscience, Brisbane, Australia; 6: Wellcome Centre for Mitochondrial Research, Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK; 7: NHS Highly Specialised Service for Rare Mitochondrial Disorders, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK; 8: The University of Queensland Diamantina Institute, Faculty of Medicine, The University of Queensland, Brisbane, Australia Mitochondria released from astrocytes contribute to the striatal neuronal vulnerability in Huntington’s disease 1: Departament de Biomedicina, Facultat de Medicina. Universitat de Barcelona, Spain; 2: Institut de Neurociències. Universitat de Barcelona, Spain; 3: Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain; 4: Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain. Mitophagy in CHCHD10 related disorders: beneficial or a deleterious pathway? Institute for Research on Cancer and Aging, Nice (IRCAN) - France Harlequin mice exhibit cognitive impairment, severe loss of Purkinje cells and a compromised bioenergetic status due to the absence of Apoptosis Inducing Factor 1: Université Paris Cité, NeuroDiderot, Inserm, F-75019 Paris, France; 2: Neonatal Research Group, Instituto de Investigación Sanitaria La Fe (IISLAFE), Valencia, Spain; 3: Department of Physiology, University of Valencia, Vicent Andrés Estellés s/n, 46100 12 Burjassot, Spain; 4: Laboratory of Comparative Neurobiology, Cavanilles Institute of Biodiversity and Evolutionary Biology, University of Valencia, Valencia, Spain; 5: Université de Paris, UMR-S 1144 Inserm, 75006 Paris, France; 6: Université Paris Cité, Platform of Cellular and Molecular Imaging, US25 Inserm, UAR3612 CNRS, 75006 Paris, France Mitochondrial dysfunction and calcium dysregulation in COQ8A-Ataxia Purkinje neurons are rescued by CoQ10 treatment 1: Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), INSERM U1258, CNRS UMR7104, Université de Strasbourg, France; 2: Institut NeuroMyoGene, UMR5310, INSERM U1217, Université Claude Bernard Lyon I Faculté de médecine, Lyon, France; 3: Institut de Biologie du Développement de Marseille (IBDM), CNRS, UMR7288, Aix-Marseille Université, Marseille, France. Macromolecular crowding: A novel player in mitochondrial physiology and disease 1: Radboud University Medical Center, The Netherlands; 2: University of Amsterdam, The Netherlands; 3: King's College, London, UK; 4: University of Twente, The Netherlands; 5: Wageningen University, The Netherlands Preserved motor function and striatal innervation despite severe degeneration of dopamine neurons upon mitochondrial dysfunction 1: Center for Physiology and Pathophysiology, Faculty of Medicine and University Hospital Cologne, Germany; 2: Medical Research Council Mitochondrial Biology Unit, University of Cambridge, UK; 3: Medical Research Council Mitochondrial Biology Unit and Department of Clinical Neurosciences, Cambridge Biomedical Campus, University of Cambridge, UK; 4: Department of Neurology, Faculty of Medicine and University Hospital Cologne, Germany; 5: Institute of Radiochemistry and Experiment Molecular Imaging, Faculty of Medicine and University Hospital of Cologne, Germany; 6: Department of Pediatrics and Adolescent Medicine, Experimental Neonatology, Faculty of Medicine and University Hospital Cologne, Germany; 7: Center for Physiology and Pathophysiology, Faculty of Medicine and University Hospital Cologne; Cologne Excellence Cluster on Cellular Stress Responses in Aging-associated Diseases (CECAD) and Center for Molecular Medicine Cologne, University of Cologne, Germany The mitochondrial DNA depletion syndrome protein FBXL4 mediates the degradation of the mitophagy receptors BNIP3 and NIX to suppress mitophagy 1: School of Biomedical Sciences, Faculty of Medicine, University of Queensland, Brisbane, Australia; 2: Department of Biotechnology, School of Biotechnology, Viet Nam National University-International University, Ho Chi Minh City, Vietnam; 3: Department of Biochemistry and Molecular Pharmacology, New York University Grossman School of Medicine, New York, USA; 4: Perlmutter Cancer Center, New York University Grossman School of Medicine, New York, USA; 5: The University of Queensland, Institute for Molecular Bioscience, Brisbane, Australia; 6: Wellcome Centre for Mitochondrial Research, Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK; 7: NHS Highly Specialised Service for Rare Mitochondrial Disorders, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK; 8: The University of Queensland Diamantina Institute, Faculty of Medicine, The University of Queensland, Brisbane, Australia Parsing universal heteroplasmy in a large maternal lineage carrying the common LHON variant m.11778G>A/MT-ND4 1: Azienda USL di Bologna - IRCCS Istituto delle Scienze Neurologiche di Bologna, Italy; 2: Department of Biomedical and Neuromotor Sciences (DIBINEM), University of Bologna, Bologna, Italy; 3: Istituto Italiano di Tecnologia – IIT, Genova, Italy; 4: Instituto de Olhos de Colatina, Colatina, Espírito Santo, Brazil; 5: Departamento de Oftalmologia e Ciências Visuais, Escola Paulista de Medicina, Universidade Federal de São Paulo (UNIFESP), São Paulo, São Paulo, Brazil; 6: Doheny Eye Institute, Los Angeles, CA, USA; Department of Ophthalmology, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA; 7: Medical Research Council Mitochondrial Biology Unit, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK PNPLA3, MBOAT7 and TM6SF2 modify mitochondrial dynamics in NAFLD patients: dissecting the role of cell-free circulating mtDNA and copy number 1: Fondazione IRCCS Cà Granda Ospedale Policlinico, Italy; 2: Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Italy; 3: Department of Pathophysiology and Transplantation, Università degli Studi di Milano, Italy The overexpression of TM6SF2 and/or MBOAT7 wild-type genes restores the mitochondrial lifecycle and activity in an in vitro NAFLD model 1: Fondazione IRCCS Cà Granda Ospedale Policlinico, Italy; 2: Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Italy; 3: Department of Pathophysiology and Transplantation, Università degli Studi di Milano, Italy |