个人简介

Ph.D. University of Manchester (UK) 1999 M.Sc.. University of Manchester (UK) 1996 B.Sc. (Hons) University of Aberdeen (UK) 1995

研究领域

Neurobiology

Understanding Neurodegenerative Mechanisms in Parkinson’s Disease Genetic cases linked with Parkinson’s disease (PD) have helped us understand how cells die in PD. Dysfunction of organelles including the proteasome, mitochondria and lysosome, as well as oxidative stress contribute to cell death in PD. We have developed cell models of PD that take into account the different factors that contribute to PD pathology to further our understanding of cell death mechanisms in sporadic and familial cases of PD. Our studies have demonstrated that mitochondria are central to the pathology of PD. On-going studies in the lab are focussed on understanding how mitochondrial dysfunction is affected in PD. We are also testing novel neuroprotective treatment targets in animal models of PD. Mechanisms Underlying Symptoms of Parkinson’s Disease In Parkinson’s disease (PD), as a consequence of slow and progressive degeneration of the dopaminergic projections from the substantia nigra pars compacta (SNc) to the striatum, function of the striatum is negatively impacted, causing dysregulation of basal ganglia circuitry, which drives abnormalities in basal ganglia function, which underpins the symptoms of PD. To understand how symptoms of PD are generated in the striatum, we are using rodent models of Parkinson’s disease to tease out the molecular and cellular abnormalities in the striatal output pathways. These studies largely involve genetic manipulation as well as biochemical and electrophysiological techniques. Specifically we are interested in determining how synaptic proteins and synaptic plasticity contribute to symptoms of PD.

近期论文

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Development of a unilaterally-lesioned 6-OHDA mouse model of Parkinson's disease.Thiele SL, Warre R, Nash JE.J Vis Exp 2012;(60) pubmed A novel MDMA analogue, UWA-101, that lacks psychoactivity and cytotoxicity, enhances L-DOPA benefit in parkinsonian primates.Johnston TH, Millar Z, Huot P, Wagg K, Thiele S, Salomonczyk D, Yong-Kee CJ, Gandy MN, McIldowie M, Lewis KD, Gomez-Ramirez J, Lee J, Fox SH, Martin-Iverson M, Nash JE, Piggott MJ, Brotchie JM.FASEB J. 2012 May;26(5):2154-63 pubmed Generation of a model of L-DOPA-induced dyskinesia in two different mouse strains.Thiele SL, Warre R, Khademullah CS, Fahana N, Lo C, Lam D, Talwar S, Johnston TH, Brotchie JM, Nash JE.J. Neurosci. Methods 2011 Apr;197(2):193-208 pubmed LTP in hippocampal neurons is associated with a CaMKII-mediated increase in GluA1 surface expression.Appleby VJ, Corrêa SA, Duckworth JK, Nash JE, Noël J, Fitzjohn SM, Collingridge GL, Molnár E.J. Neurochem. 2011 Feb;116(4):530-43 pubmed Altered function of glutamatergic cortico-striatal synapses causes output pathway abnormalities in a chronic model of parkinsonism.Warre R, Thiele S, Talwar S, Kamal M, Johnston TH, Wang S, Lam D, Lo C, Khademullah CS, Perera G, Reyes G, Sun XS, Brotchie JM, Nash JE.Neurobiol. Dis. 2011 Mar;41(3):591-604 pubmed Disruption of the interaction between myosin VI and SAP97 is associated with a reduction in the number of AMPARs at hippocampal synapses.Nash JE, Appleby VJ, Corrêa SA, Wu H, Fitzjohn SM, Garner CC, Collingridge GL, Molnár E.J. Neurochem. 2010 Feb;112(3):677-90 pubmed To serve and protect? Interventions in the subthalamic nucleus for Parkinson's disease. Commentary on "Ablation of the subthalamic nucleus protects dopaminergic phenotype but not cell survival in a rat model of Parkinson's disease".Kalia SK, Nash JE, Lozano AM.Exp. Neurol. 2004 Feb;185(2):201-3 pubmed Characterisation of striatal NMDA receptors involved in the generation of parkinsonian symptoms: intrastriatal microinjection studies in the 6-OHDA-lesioned rat.Nash JE, Brotchie JM.Mov. Disord. 2002 May;17(3):455-66 pubmed Interaction of SAP97 with minus-end-directed actin motor myosin VI. Implications for AMPA receptor trafficking.Wu H, Nash JE, Zamorano P, Garner CC.J. Biol. Chem. 2002 Aug;277(34):30928-34 pubmed