Dr. Rocha focuses on how age-dependent changes in autophagy and lysosomal degradation pathways impact the onset of neurodegenerative diseases. Using a variety of in vitro and in vivo approaches Dr. Rocha aims to understand how lysosomal dysfunction can impact protein aggregation. Dr. Rocha is also interested in developing therapeutic targets and testing novel small-molecules to alter age-related lysosomal dysfunction. The overall goal is to prevent, or slow age-related decline associated with neurodegenerative diseases.
Education & Training
- PhD, Carleton University, Ottawa, Canada, Behavioral Neuroscience
- Post Doc Research Fellow, Neurodegeneration Research Institute, Mclean Hospital, Harvard Medical School, Belmont, MA, Neuroscience
- Post Doc Research Fellow, Pittsburgh Institute of Neurodegenerative diseases, University of Pittsburgh, PA Neuroscience / Neurodegenerative Diseases
Specialized Areas of Clinical, Research and/or Educational Interests
- Research: Autophagy – Lysosomal pathway in Neurodegeneration; Parkinson’s disease; Protein accumulation; Endosomal trafficking.
Professional Organization Membership
- Society for Neuroscience
Honors & Awards
- Graduate Award for Ontario Students for Research in Dementia
- Society for Neuroscience Graduate Student Travel Award
- Canadian Institute of Health Research Post-Doctoral Fellowship
- American Parkinson’s disease Foundation Fellowship
- Parkinson’s disease Foundation Postdoctoral Fellowship
Selected Recent Publications
Rocha, EM, Smith, GA, Park E, Cao H, Graham A, Brown H, Hayes, MA, Beagan, JA, McLean JR, Izen, SC, Perez-Torres, EJ, Hallett, PJ, Isacson, O. (2015) Chronic pharmacological glucocerebrosidase inhibition induces -synuclein aggregation, microglial and complement activation and synaptic protein changes in mice. Antioxidant Redox Signaling.; 20;23(6):550-64.
Rocha EM, Smith GA, Park E, Cao H, Brown E, Hayes MA, Beagan J, McLean JR, Izen SC, Perez-Torres E, Hallett PJ, and Isacson O. (2015) Glucocerebrosidase gene therapy prevents -synucleinopathy of midbrain dopamine neurons. Neurobiology of Disease.; 82:495-503.
Di Maio, R., Hoffman,E.K., Rocha, E.M., Keeney, M.T., Sanders, L.H., De Miranda, B.R., Zharikov, A., Van Laar, A., McCoy, J. Stepan, A.F., Lanz, T.A., Kofler, J.K., Burton, E.A., Alessi, D.R., Hastings, T.G., Greenamyre, J.T. (2018) LRRK2 activation in idiopathic Parkinson Disease. Science Translational Medicine.; 10(451).
Rocha EM, De Miranda B, Sanders LH. (2018) Alpha-synuclein: Pathology, mitochondrial dysfunction and neuroinflammation in Parkinson’s disease. Neurobiology of Disease.; 109(Pt B):249-257.
Rocha EM, De Miranda BR, Castro S, Drolet R, Hatcher NG, Yao L, Smith SM, Keeney MT, Di Maio R, Kofler J, Hastings TG, Greenamyre JT. (2018) LRRK2 inhibition prevents endolysosomal deficits seen in human Parkinson's disease. Neurobiology of Disease. Feb;134:104626. doi: 10.1016/j.nbd.2019.104626., 2020