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Faculty Detail    
Name JEREMY H HERSKOWITZ
  
Campus Address SHEL 912 Zip 2182
Phone  (205) 996-6329
E-mail  jhersko@uab.edu
Other websites Herskowitz Lab Website
     


Faculty Appointment(s)
Appointment Type Department Division Rank
Secondary  Neurobiology  Neurobiology Assistant Professor
Center  Comprehensive Neuroscience Center  Comprehensive Neuroscience Center Associate Professor
Center  Ctr Neurodegeneration & Exp Ther (CNET)  Ctr Neurodegeneration & Exp Ther (CNET) Associate Professor
Center  Alzheimer's Disease Center  Alzheimer's Disease Center Associate Professor
Center  Evelyn F. McKnight Brain Institute  Evelyn F. McKnight Brain Institute Associate Professor
Center  Civitan International Research Center  Civitan International Research Center Associate Professor
Primary  Neurology Chair Office  Neurology Chair Office Associate Professor

Graduate Biomedical Sciences Affiliations
Cell, Molecular, & Developmental Biology 
Medical Scientist Training Program 
Neuroscience 
Neuroscience Graduate Program 
Neurosciences 

Biographical Sketch 
Dr. Herskowitz received his B.S. in Chemistry from the University of North Carolina at Chapel Hill in 2001. He earned a Ph.D in Microbiology at Emory University, where he studied mechanisms of gammaherpesvirus pathogenesis in the laboratory of Dr. Samuel Speck. He remained at Emory University for postdoctoral studies and conducted basic research in the laboratory of Drs. James Lah and Allan Levey at the Center for Neurodegenerative Disease, investigating cellular and animal models of Alzheimer’s disease. He was appointed as an Instructor of Neurology at Emory University in 2012. In 2014, he moved to UAB where he is now Assistant Professor of Neurology and Neurobiology and the Collat Scholar in Neuroscience.

Society Memberships
Organization Name Position Held Org Link
Society for Neuroscience    http://www.sfn.org/ 
 



Research/Clinical Interest
Title
Neurobiology of Alzheimer's Disease
Description
The Herskowitz lab studies the neurobiology of Alzheimer Disease (AD) with a focus on understanding the underlying cellular and molecular mechanisms that will lead to better treatments. We apply modern neuroscience approaches to study animal and cellular models of AD. We have shown that inhibiting Rho kinase signaling with small molecules substantially reduces the production of amyloid in experimental AD models, and we are continuing to use a variety of behavioral, electrophysiological, and biochemical approaches to better understand this protective effect. Other efforts of the lab include basic, fundamental neuroscience research examining how cognition is influenced by structural plasticity of dendritic spines.

Selected Publications 
Publication PUBMEDID
Herskowitz JH, Feng Y, Mattheyses AL, Hales CM, Higginbotham LA, Duong DM, Montine TJ, Troncoso JC, Thambisetty M, Seyfried NT, Levey AI, Lah JJ. Pharmacologic inhibition of ROCK2 suppresses amyloid-β production in an Alzheimer disease mouse model. Journal of Neuroscience. 33(49): 19086-98, 2013.  22621900 
Herskowitz JH, Seyfried NT, Gearing M, Kahn RA, Peng J, Levey AI, Lah JJ. Rho kinase II phosphorylation of the lipoprotein receptor LR11/SorLa alters amyloid-β production. Journal of Biological Chemistry. 286: 6117-27, 2011.
 		 21147781 
Herskowitz JH, Offe K, Deshpande A, Kahn RA, Levey AI, Lah JJ. GGA1-mediated endocytic traffic of LR11/SorLA alters APP intracellular distribution and amyloid-β production. Molecular Biology of the Cell. 14: 2645-57, 2012.   24305806 
Herskowitz JH, Gozal YM, Duong DM, Dammer EB, Gearing M, Ye K, Lah JJ, Peng J, Levey AI, Seyfried NT. Asparaginyl endopeptidase cleaves TDP-43 in brain. Proteomics. 12: 2455-63, 2012.  22718532 
Herskowitz JH, Seyfried NT, Duong DM, Xia Q, Rees HD, Gearing M, Peng J, Lah JJ, Levey AI. Phosphoproteomic analysis reveals site-specific changes in GFAP and NDRG2 phosphorylation in frontotemporal lobar degeneration. Journal of Proteome Research (ACS). 9: 6368-79, 2010.  20886841 
Sager KL, Wuu J, Herskowitz JH, Mufson EJ, Levey AI, Lah JJ. Neuronal LR11 expression does not differentiate between clinically-defined Alzheimer’s disease and control brains. PLOS ONE. 7(8):e40527, 2012.  22927900 
 

Keywords
Neurodegeneration, Alzheimer's disease, amyloid, signaling, plasticity, behavior, neuroscience, cell biology