Professor Benjamin Wolozin

Benjamin Wolozin, M.D., Ph.D. is Professor, Department of Pharmacology, Alzheimer's Disease Center, Boston University.
 
Ben's interests focus on the pathophysiology of Alzheimer's and Parkinson's disease.
 
His work on Alzheimer's disease examines the role of cholesterol in the pathophysiology of Alzheimer's disease, and stems from his discovery in 2000 that subjects taking the cholesterol lowering medicines, termed statins, have a lower incidence of Alzheimer's disease.
 
His work on Parkinson's disease examines the interaction between genes implicated in the disease, such as parkin and a -synuclein, and environmental factors implicated in the disease. He uses a wide range of approaches to study neurodegenerative disease ranging from molecular approaches to epidemiology. These approaches include molecular biology, cellular biology, transgenic mice, transgenic C. elegans, study of human brain samples, and epidemiological database analyses.
 
At present, Ben serves as the primary investigator for several funded studies including, Regulation of Amyloid Precursor Protein Processing by Presenilins, Regulation of Ubiquitination and Receptor Signaling by Parkin, Mechanisms of a-synuclein aggregation and toxicity, and Epidemiological Screen for Medicines that Modify the Course of Alzheimer's disease.
 
Ben has received numerous awards for his research including the Donald B. Lindsley Prize, Society for Neuroscience, the A. E. Bennett Award, and a Merit Award from Alzforum. He serves on numerous editorial boards, including for the Journal of Biological Chemistry and Neurodegenerative Diseases, and is a standing member of the NIH CDIN study section.
 
He coauthored the innovative Amazon download Is CABG associated with an increased risk of neurocognitive degeneration?, and coauthored α-Synuclein Shares Physical and Functional Homology with 14-3-3 Proteins, Presenilin 1 associates with glycogen synthase kinase-3β and its substrate tau, The A53T α-Synuclein Mutation Increases Iron-Dependent Aggregation and Toxicity, Aggregated and Monomeric α-Synuclein Bind to the S6' Proteasomal Protein and Inhibit Proteasomal Function, CHIP and Hsp70 regulate tau ubiquitination, degradation, and aggregation, and Requirement of the Familial Alzheimer's Disease Gene PS2 for Apoptosis: Opposing Effect of ALG-3.
 
Ben completed his undergraduate education at Wesleyan University in Middletown, CT. He earned his M.D. and Ph.D. degrees from Albert Einstein College of Medicine, as part of the Medical Scientist Training Program. His postdoctoral fellowships were spent at Mt. Sinai Medical Center (1988-1989) and the National Institute of Mental Health (1989-96). He joined Loyola University Medical Center in 1996 as an Associate Professor and rose to the rank of tenured full professor. He joined the Boston University School of Medicine's Department of Pharmacology in 2004 as a Professor and is currently obtaining an adjunct position in the Department of Neurology.
 
Read Alzforum: The Forum Interviews: Benjamin Wolozin, Statins that stave off Alzheimer's (Zocor), High Cholesterol In Midlife Raises Risk Of Late-Life Dementia, Study Finds, and Angiotensin receptor blockers associated with lower risk of Alzheimer's disease. Visit Ben's Facebook page and his LinkedIn page.