Benjamin Wolozin, MD, PhD
Professor, Department of Pharmacology
Location: Housman, R614
Benjamin Wolozin 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 (1988-9) 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 Dept. of Neurology.
Dr. Wolozin’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, Dr. Wolozin 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 .
Dr. Wolozin 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.
Recent peer-reviewed publications of Dr. Wolozin’s work include:
Wolozin, B.L. ,et al: Participation of Presenilin-2 in apoptosis: Enhanced basal activity conferred by Alzheimer mutation. Science, 274:1710-1713, 1996.
Wolozin, B.L. , Kellman, W., Ruosseau, P., Celesia, G.G. and Siegel, G.: Decreased prevalence of Alzheimer’s disease, Associated with HMG-CoA reductase inhibitors. Archives Neurol., 57: 1439-1443, 2000.
Pappolla MA, Bryant-Thomas TK, Herbert D, Pacheco J, Fabra Garcia M, Manjon M, Girones X, Henry TL, Matsubara E, Zambon D, Wolozin B, Sano M, Cruz-Sanchez FF, Thal LJ, Petanceska SS, Refolo LM. Mild hypercholesterolemia is an early risk factor for the development of Alzheimer amyloid pathology. Neurology.61:199-205 (2003).[PubMed]
Petrucelli, L., Dickson, D., Kehoe, K., Taylor, J., Snyder, H., Grover, A., McGowan, E., Lewis, J., Dillman, W., Browne, S.E., Voellmey, R., Tsuboi, Y., Dawson., T.M., Wolozin, B., Hardy, J., Hutton, M., CHIP and Hsp70 regulate tau ubiquitination, degradation and aggregation. Human Molecular Genetics 13:703-14(2004). [PubMed]
Brown, J., Theisler, C., Silberman, S., Magnuson, D., Russell, D.W., Marquez-Sterling, N., Lee, J.M., Yager, D., Crowley, J., Sambamurti, K., Rahman, M., Reiss, A.B., Eckman, C.B., Wolozin, B ., Differential Expression of Cholesterol Hydroxylases in Alzheimer’s disease. JBC 279: 34674-81 (2004). [PubMed]
Frasier, M, Walzer, M, McCarthy, L, Magnuson, D, Lee, JM, Haass, C, Kahle, P, Wolozin, B. Tau phosphorylation increases in symptomatic mice over-expressing A30P a -synuclein. Exp. Neurol. In press (2005). [PubMed]
Poon, HF, Frasier, M, Sherve, N, Calebrese, V, Wolozin, B, Butterfield, AD, Mitochondrial associated Metabolic Proteins are Selectively Oxidized in A30P -Synuclein Transgenic Mice – A Model of Familial Parkinson’s Disease, Neurobio. Dis. (In press). [PubMed]