Ghazaleh Sadri-Vakili

Ghazaleh is an Assistant Professor of Neurology at the Harvard Medical School and Assistant in Neuroscience at the Massachusetts General Hospital. She received her Ph.D. from Boston University School of Medicine in Pharmacology and Biomedical Neuroscience and completed her postdoctoral studies at the Massachusetts General Hospital.

Research Narrative

The NeuroEpigenetics laboratory at MIND, under the direction of Ghazaleh Sadri-Vakili studies the molecular mechanisms that underlie alterations in gene expression in disorders of the nervous system using the most current molecular biology tools.

Currently, their efforts are focused on Huntington’s disease (HD), Amyotrophic Lateral Sclerosis (ALS), as well as addiction.

So far, they have identified a number of epigenetic alterations, or those that don’t involve changes in the DNA sequence, that lead to changes in gene expression in animal and cellular models of HD and are targeting histone modifying enzymes such as histone deacetylases as a novel approach for the treatment of HD.

In addition, the laboratory is currently assessing the neuroprotective effects of a novel class of compounds known as MicroNeurotrophins for the treatment of ALS and HD. The lab is also interested in investigating the molecular mechanisms that underlie drug abuse as part of several collaborations with colleagues from the University of Pennsylvania and Florida State University.

Their research is aimed at identifying the epigenetic marks and the molecular mechanisms that underlie relapse. The most recent project is focused on how exposure to drugs alters the epigenome and whether these changes are heritable by the offspring across multiple generations in models of addiction.

Research Interests

als biomarkers; amyotrophic lateral sclerosis; epigenetics; huntington disease; substance use disorder; therapeutics; x-linked dystonia parkinsonism

Education

• PhD Boston University 2003

Selected Publications

Famous, K.R., Kumaresan, V., Sadri-Vakili, G., Schmidt, H.D., Mierke, D.F., Cha, J.-H.J., and Pierce, R.C. Phosphorylation-dependent trafficking of GluR2-containing AMPA receptors in the nucleus accumbens shell contributes to the reinstatement of cocaine seeking. Journal of Neuroscience 2008; 28(43):11061-70.

Benn, C.L., Luthi-Carter, R., Kuhn A., Sadri-Vakili, G., Blankson, K.L., Dalai, S.C., Goldstein, D.R., Spires, T.L., Pritchard, J., Olson, J.M., van Dellen, A., Hannan, A.J., Cha, J.-H.J. Environmental enrichment reduces neuronal intranuclear inclusion load but has not effect on mRNA expression in a mouse model of Huntington’s disease. Journal of Neuropathology and Experimental Neurology 2010; 69(8):817-27.

Sadri-Vakili, G., Kumaresan, V., Schmidt, H.D., Famous, K.R., Chawla, P., Vassoler, F., Xia, E., Overland, R.P., Bass, C.E., Terwilliger, E.F., Pierce, R.C., and Cha, J.H.J. Cocaine-induced chromatin remodeling increases brain-derived neurotrophic factor transcription in the rat medial prefrontal cortex, which alters the reinforcing efficacy of cocaine. Journal of Neuroscience 2010; 30(35):11735-11744.

McCarthy, D., Zhang, X., Darnell, S.B., Sangrey, G.R., Yanagawa, Y., Sadri-Vakili, G., and Bhide, P.G. (2011) Cocaine alters BDNF expression and neuronal migration in the embryonic mouse forebrain. Journal of Neuroscience 31:13400-13411.