Cellular processing of Alpha-synuclein : implications for Parkinson’s Disease

Mark Cooper

Dr Mark Cooper trained in the field of mitochondrial biochemistry in disease under the supervision of Dr John Morgan-Hughes and Professor John Clark (PhD 1987) at the Institute of Neurology, London. Dr Cooper was appointed as Lecturer in the Department of Protein and Molecular Biology at the Royal Free Hospital Medical School, and subsequently in 1994 as Senior Lecturer in the department of Clinical Neurosciences. In 2010 he was appointed as Reader in Neurodegenerative diseases in the department of Clinical Neurosciences, UCL Institute of Neurology.

Dr Cooper’s work on Parkinson’s Disease (PD) focuses on elucidating the cell and molecular mechanisms underlying the disease. Over the past 20 years his research has focussed on the role of mitochondrial dysfunction in PD brains (Schapira et al 1990) and platelets (Krige et al 1994) and its relationship to other features detected in PD brains including: mitochondrial DNA defects (Gu et al 1998), nitric oxide (Cleeter et al 1994), oxidative stress (Seaton et al 1997), iron (Hartley et al 1993) and cell death (Hartley et al 1994). Increasingly with the identification of the familial causes of PD his research has turned to the role of specific mutant genes in PD pathogenesis. Alpha-synuclein has been the main focus of his research with additional interests in: LRRK2 (Papkovskaia et al 2012), parkin (Gegg et al 2010) and glucocerebrosidase (Gegg et al 2012). While mitochondrial biochemistry is a recurrent theme he also has a broader interest in dopamine metabolism (Tabrizi et al 2000), protein degradation pathways (Alvarez-Erviti et al 2010), alpha-synuclein aggregation and transmission (Alvarez-Erviti et al 2011) and microRNA dysregulation (Alvarez-Erviti et al 2013). Dr Mark Cooper is also interested in Friedreich’s Ataxia, Huntingdon’s disease and mitochondrial abnormalities.