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Antony Cooper

Professor
Neuroscience
Garvan Institute of Medical Research
Australia

Biography

Antony Cooper is a cell and molecular biologist / geneticist with strong interests in elucidating how cellular dysfunction results in human diseases, with a specific interest in neurodegenerative disease such as Parkinson’s Disease. His research on neurodegenerative diseases focuses on understanding the basis of Parkinson’s Disease. Antony completed a PhD at McGill University working on membrane trafficking, and post-doctoral studies at the University of Oregon involving both protein splicing and proteostasis/protein quality control in the endoplasmic reticulum (ER). As an Assistant Professor at the University of Missouri his interests evolved to protein misfolding, ER stress and oxidative stress, factors common to many neurodegenerative diseases. As a tenured Associate Professor in Missouri and since returning to Australia at the Garvan Institute he has focused his research on Parkinson’s disease.

Research Interest

Parkinson’s Disease; discovering the cause and new approaches to diagnose, treat and cure Neurogenomics; identifying the genomic and transcriptomic contribution to neurodegenerative diseases Proteostasis - the integrated cellular pathways that control the biogenesis, folding, trafficking and degradation of proteins Cellular stresses such as oxidative and nitrosative stress/damage, stress in the endoplasmic reticulum, hypoxia and how they disrupt proteostasis

Publications

  • Murphy KE; Gysbers AM; Abbott SK; Tayebi N; Kim WS; Sidransky E; Cooper A; Garner B; Halliday GM, 2014, 'Reduced glucocerebrosidase is associated with increased α-synuclein in sporadic Parkinson's disease', Brain: a journal of neurology, vol. 137, no. 3, pp. 834 - 848

  • Protter D, Lang C, Cooper AA. αSynuclein and Mitochondrial Dysfunction: A Pathogenic Partnership in Parkinson's Disease? Parkinsons Dis. 2012

  • Murphy KE; Gysbers AM; Abbott SK; Spiro AS; Furuta A; Cooper A; Garner B; Kabuta T; Halliday GM, 'Lysosomal-associated membrane protein 2 isoforms are differentially affected in early Parkinson's disease', Movement Disorders, 2015; vol. 30, no. 12, pp. 1639 - 1647.

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