Position(s):
Assistant Professor, Dept. of Bioscience & Biotechnology
Assistant Professor, Dept. of Biochemistry & Molecular Biology, 
                               Drexel University College of Medicine.
Director - Drexel University RNAi Resource Center 

Office: 316 Stratton Hall
Lab: 308 Stratton Hall

Phone: (215) 895-6772 (Office)
            (215) 895-6884 (Lab)

Email: ajs56@drexel.edu

B.S. - Pennsylvania State University
Ph.D. - University of North Carolina, Chapel Hill

Courses Taught

BIO218: Principles of Molecular Biology
BIO219: Principles of Molecular Biology Laboratory
BIO412: Biology of Aging
BIO463/663: Molecular Mechanisms of Neurodegeneration
BIO540: Readings in Biochemistry, Cellular and Molecular Biology

The two greatest risk factors for Alzheimer’s disease (AD) are increasing age and family history of AD. In my laboratory we are interested in understanding the mechanism by which increasing age and family history lead to this increased risk. To facilitate our goal, we utilize biochemical, genetic, cell and molecular biology techniques. Specifically we take advantage of genetic association studies and functional assays to identify proteins involved in AD pathophysiology. We then characterize these proteins in cell culture and transgenic mouse model systems of AD to yield insight into the disease mechanism. Abundant genetic, biochemical, and neuropathological evidence implicates the accumulation of the b-amyloid (A b) peptide to be the key event in AD. Ab is produced by the proteolytic processing of the amyloid precursor protein (APP). Currently in the lab we are developing and implementing a genome-wide, RNA interference based screen for proteins that modulate APP proteolytic processing. To facilitate this approach, we have established the Drexel University RNAi Resource Center which provides shRNA based knockdown plasmids that target over 28,000 human genes. We are also characterizing individual proteins that have been genetically implicated in AD. Alpha-2-macroglobulin (A2M) facilitates A b degradation and we have identify polymorphisms in this gene that increase the risk for AD. We are functionally characterizing these variant proteins. KIFF11 is a kinesin motor protein that is genetically implicated in AD. We are determining if KIFF11 is involved in the axonal transport of APP. Finally, caloric restriction is the only non-genetic intervention that slows aging and extends lifespan. We are investigating the role of regulators of caloric restriction on AD pathogenesis.

Post-Docs and Graduate Students

Can (Martin) Zhang: Development of RNAi-based assay to identify novel modulators of
                              APP processing.
Preeti Khandelwal: Development of RNAi-based assay to identify novel modulators of
                            APP processing.
Ranjita Mukherjee: The effects of nutrient availability on APP processing.
Neha Patel: Investigating the role of micro-RNAs in APP gene regulation.
Sara Ansaloni: Kiff11-mediated axonal transport.

Personal/Laboratory Website(s):