Conference Agenda

Destructuring of mitochondrial cristae in the initiation of CHCHD10-related neurodegeneration

Véronique Paquis-Flucklinger^1,2

¹IRCAN, UMR 7284/INSERM U1081/UCA, Nice, France; ²Reference Center for mitochondrial diseases, Universitary hospital, Nice, France

Convergence of mitochondrial and lysosomal dysfunction in Parkinson’s disease

Lena F Burbulla

Ludwig Maximilian University (LMU) Munich, Germany

Development of cortical organoids to model m.3243A>G disease and understand cell specificity

Denisa Hathazi, Yu Nie, Camilla Lions, Juliane Müller, George Gibbons, Patrick Chinnery, Andras Lakatos, Rita Horvath

University of Cambridge, United Kingdom

Brain and brainstem-specific mitochondrial diversity associated with vulnerability to neurodegeneration in mitochondrial diseases

Anna S. Monzel¹, Masashi Fujita², Ayelet M. Rosenberg¹, Eugene V. Mosharov^3,6, Jack Devine¹, David A. Bennett^4,5, Vilas Menon², Philip L. De Jager², Martin Picard^1,6,7

¹Division of Behavioral Medicine, Department of Psychiatry, Columbia University Irving Medical Center, New York NY, USA; ²Center 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; ³Division of Molecular Therapeutics, Department of Psychiatry, Columbia University Irving Medical Center, New York NY, USA; ⁴Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL, USA; ⁵Department of Neurological Sciences, Rush University Medical Center, Chicago, IL, USA; ⁶New York State Psychiatric Institute, New York NY, USA; ⁷Department of Neurology, Columbia University Irving Medical Center, New York NY, USA

Mitochondrial DNA mutations exacerbate motor and behavioural deficits in a mouse model of Parkinson’s disease

Michael J Keogh^1,2, Yu Nie^2,3, Zoe Golder^2,3, Malwina Prater^2,3, Nils-Goran Larsson⁴, Andrew Blamire^1,5, Chris Morris¹, Patrick F Chinnery^2,3

¹Clinical and Translational Research Institute, Centre for Life, Newcastle University, UK, NE3 1BZ; ²Department of Clinical Neuroscience, University of Cambridge, UK, CB2 0QQ; ³Medical Research Council Mitochondrial Biology Unit, University of Cambridge, UK, CB2 0QQ; ⁴Division of Molecular Metabolism, Biomedicum, floor 9D, Solnavägen 9, Karlolinska Institute, 171 65 Stockholm, Sweden; ⁵Newcastle Magnetic Resonance Centre, Campus for Ageing and Vitality, Newcastle University, NE4 5PL

Macromolecular crowding: A novel player in mitochondrial physiology and disease

Elianne P Bulthuis¹, Cindy EJ Dieteren¹, Jesper Bergmans¹, Job Berkhout¹, Jori A Wagenaars¹, Els MA van de Westerlo¹, Emina Podhumljak¹, Mark A Hink², Laura FB Hesp¹, Hannah S Rosa³, Afshan N Malik³, Mariska Kea-te Lindert¹, Peter HGM Willems¹, Han JGE Gardeniers⁴, Wouter K den Otter⁴, Merel JW Adjobo-Hermans¹, Werner JH Koopman^1,5

¹Radboud University Medical Center, The Netherlands; ²University of Amsterdam, The Netherlands; ³King's College, London, UK; ⁴University of Twente, The Netherlands; ⁵Wageningen University, The Netherlands

Preserved motor function and striatal innervation despite severe degeneration of dopamine neurons upon mitochondrial dysfunction

Thomas Paß¹, Roy Chowdury², Julien Prudent², Yu Nie³, Patrick Chinnery³, Markus Aswendt⁴, Heike Endepols⁵, Bernd Neumaier⁵, Trine Riemer⁶, Bent Brachvogel⁶, Rudi Wiesner⁷

¹Center for Physiology and Pathophysiology, Faculty of Medicine and University Hospital Cologne, Germany; ²Medical Research Council Mitochondrial Biology Unit, University of Cambridge, UK; ³Medical Research Council Mitochondrial Biology Unit and Department of Clinical Neurosciences, Cambridge Biomedical Campus, University of Cambridge, UK; ⁴Department of Neurology, Faculty of Medicine and University Hospital Cologne, Germany; ⁵Institute of Radiochemistry and Experiment Molecular Imaging, Faculty of Medicine and University Hospital of Cologne, Germany; ⁶Department of Pediatrics and Adolescent Medicine, Experimental Neonatology, Faculty of Medicine and University Hospital Cologne, Germany; ⁷Center 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

Keri-Lyn Kozul¹, Giang Thanh Nguyen-Dien^1,2, Yi Cui¹, Prajakta Gosavi Kulkarni¹, Michele Pagano^3,4, Brett M. Collins⁵, Robert Taylor^6,7, Mathew J.K. Jones⁸, Julia K. Pagan^1,5,8

¹School of Biomedical Sciences, Faculty of Medicine, University of Queensland, Brisbane, Australia; ²Department of Biotechnology, School of Biotechnology, Viet Nam National University-International University, Ho Chi Minh City, Vietnam; ³Department of Biochemistry and Molecular Pharmacology, New York University Grossman School of Medicine, New York, USA; ⁴Perlmutter Cancer Center, New York University Grossman School of Medicine, New York, USA; ⁵The University of Queensland, Institute for Molecular Bioscience, Brisbane, Australia; ⁶Wellcome Centre for Mitochondrial Research, Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK; ⁷NHS Highly Specialised Service for Rare Mitochondrial Disorders, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK; ⁸The University of Queensland Diamantina Institute, Faculty of Medicine, The University of Queensland, Brisbane, Australia