A/Prof. Antony Cooper
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.Assoc Professor Antony Cooper is a Parkinson’s Disease scientist who completed his PhD at McGill University in Montreal before undertaking post-doctoral studies at the Institute of Molecular Biology at the University of Oregon where he investigated protein misfolding, cellular quality control, mitochondrial dysfunction and associated damaging reactive oxygen species. These features coalesce prominently in Parkinson’s Disease and while a tenured faculty member at the University of Missouri he re-directed his research focus to identify the underlying molecular mechanisms of the disease. He returned to Australia in 2006 to join the Garvan Institute of Medical Research in Sydney where he has continued investigating the molecular mechanisms of the disease with emphasis on alpha-synuclein, a protein with a central toxic role in Parkinson’s Disease, and how it relates to known problems within the cells of patients. Current major research directions he is pursuing include:
1. Disease progression. The protein alpha-synuclein can assume an alternative shape that is toxic to neurons and which can be released from neurons, transfers to adjacent neurons and transforms αSyn in recipient cells in a process thought to be a major contributor to the progression (worsening) of the disease. Halting this neuron-toneuron transmission by reducing the release of toxic αSyn is a strong therapeutic possibility to inhibit disease progression.
2. Biomarkers (reporters of disease status). Validation studies are currently underway using RNA from patients blood to assess the biomarker’s accuracy in identifying previously diagnosed patients. If successful, these biomarkers will be tested to assess if they can identify patients much earlier in the disease course.
3. Collaboratively investigating the contribution of genetic changes as an underlying contributor to idiopathic Parkinson’s Disease.
Attempted 300 character bio (299):
Parkinson’s Research scientist. PhD (McGill, Canada), Post-Doc (Oregon), Faculty (Missouri). Returned to Australia to the Garvan Institute (Sydney) to study the molecular mechanisms of Parkinson’s Disease, Biomarkers, Genetic contributions and the intent of slowing/stopping disease progression