Mitochondrial dysfunction and therapeutic potential

Mitochondrial dysfunction and therapeutic potential: Session convened by Parkinson’s UK
Theme: Parkinson's disease and other neurodegenerative disorders
Part of the Parkinson’s UK Programme Stream
Sunday 23rd April, 10:20 – 12:00

Mitochondrial dysfunction is common to a variety of neurodegenerative disorders, including Parkinson's which is the fastest growing neurodegenerative disorder. Since the initial discovery of mitochondrial complex I deficiency and reduced ATP levels in the substantia nigra from Parkinson's brain donors compared to healthy donors, growing evidence further supports problems with mitochondrial bioenergetics, mitochondrial dynamics and trafficking etc. Additionally, gene mutations e.g. PINK1 etc. known to cause familial forms of Parkinson's have been demonstrated to impact on mitochondrial function. This adds further support to the hypothesis that mitochondrial dysfunction is core to the pathological process in Parkinson's and hence mitochondria are a suitable drug target for disease modifying therapies.

Niamh Connolly, Royal College of Surgeon Dublin, Ireland: Mitochondrial bioenergetics, dynamics, morphology and stress response in neurons exposed to alpha-synuclein preformed fibrils (co-chair)

 Biography: Niamh is a lecturer at the Centre for Systems Medicine in RCSI University of Medicine & Health Services, Dublin. Her research is interdisciplinary, applying computational and experimental approaches to investigate mitochondrial and bioenergetic dysfunction in neurodegenerative diseases including Parkinson’s and Alzheimer’s (


Olga Corti, Paris Brain Institute (Institut du Cerveau), Paris: Mitochondrial dysfunction in the alpha-synuclein preformed fibril mouse model of Parkinson’s disease

Miratul Muqit, MRC Protein phosphorylation and ubiquitylation unit, Dundee: Decoding Mitochondrial Damage Response Pathways linked to Parkinson’s disease (co-chair)

Heather Mortiboys, SiTRaN at the University of Sheffield, UK: Targeting mitochondria for disease modification in Parkinson's Disease

 Biography: Professor Heather Mortiboys received her PhD in Neuroscience (grade summa cum laude) from the International Max Planck PhD Program in Dresden Germany. She joined the Neuroscience department at the University of Sheffield in 2006 to set up mitochondrial investigations in models of Parkinson’s disease. She became a Parkinson’s UK Senior Research Fellow in 2013 to expand this work and form her own research group. She became Professor of Cellular Neuroscience and Metabolism in January 2021. Her research interests are focused on mitochondria in neurodegenerative diseases, primarily Parkinson’s disease. Her current research has two streams, understanding the mechanisms leading to cell death focusing on mitochondrial morphology, recycling, function, calcium handling, mitochondrial DNA and associated pathways as well as discovering small molecules to target these mechanisms. The research focuses on using patient derived cells to model the disease and assess novel therapeutic approaches. Her research team investigates a personalized medicine approach to disease, stratifying patients dependent on cellular phenotype and response to compound treatment. She has pioneered dopaminergic neuron culture from patients with a high dopaminergic yield and the use of high content imaging for identification of mitochondrial abnormalities in PD and subsequently compounds to improve mitochondrial function. Alongside her research she has active links with several PPI groups and is an advocate for including PPI in all research projects.

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