Benjamin Wolozin, MD, PhD
Boston University School of Medicine
Dept of Pharmacology & Experimental Therapeutics

MD, Albert Einstein College of Medicine

Dr. Wolozin’s research examines the pathophysiology of neurodegenerative diseases, including Alzheimer’s disease, Amyotrophic Lateral Sclerosis and Parkinson’s disease. His laboratory is currently focused on the role of RNA binding proteins and translational regulation in disease processes.

Parkinson’s disease: The research on Parkinson Disease focuses on genetic factors implicated in Parkinson’s disease, including LRRK2, a-synuclein, parkin, PINK1 and DJ-1. Research in our laboratory suggests that genetic mutations linked to Parkinson’s disease act by converging on a biological system that integrates the stress response, regulating autophagy, protein translation and mitochondrial function. Using genetically modified cells (e.g., primary neuronal cultures or cell lines) and genetically modified animals (C. elegans and mice), we have demonstrated that a-synuclein and LRRK2 enhance the sensitivity of dopaminergic neurons to mitochondrial dysfunction. Our work points to particular biochemical pathways mediating the actions of LRRK2. We have recently demonstrated that LRRK2 binds to MKK6, a kinase that lies upstream of p38 and regulates the stress response. LRRK2 regulates membrane localization of its binding proteins, including MKKs, JIPs, rac1 (a small GTPase) and other important proteins mediating the stress response. This work has direct relevance to therapy because it points to chemicals that might protect dopaminergic neurons and modify the course of Parkinson’s disease. For instance, we are investigating the action of SirT1 agonists (such resveratrol, the compound found in red wine or SRT1720, produced by Sirtris Pharmaceuticals), which stimulate synthesis of anti-oxidant enzymes and appear to offer protection in animal models of Parkinson’s disease. We are also investigating the action of brain penetrant analogues of rapamycin, which stimulate the neuron to remove protein aggregates, and offer neuroprotection through mechanisms complementary to SirT1.

Amyotrophic Lateral Sclerosis (ALS): Our current work focuses on a protein, TDP-43, that was recently shown to be the predominant protein that accumulates during the course of the disease. We have shown that TDP-43 is a stress granule protein, and that TDP-43 pathology co-localizes with other stress granule markers in spinal cords of subjects with ALS, as well as those with Frontotemporal Dementia. We are currently examining how TDP-43 and disease-linked mutations in TDP-43 modify synaptic function in neuronal arbors. We are using protein binding assays (immunoprecipitation, mass spectrometry) and imaging assay (fixed cells and live cell imaging) to determine the effects of TDP-43 and its mutations. We use cell lines, primary cultures of hippocampal neurons and human brain samples for our studies.

We also have an active drug discover program related to TDP-43. This program utilizes cells that inducibly over-express TDP-43, as well as lines of C. elegans expressing TDP-43 and studies in primary cultures of hippocampal neurons. We examine the compounds using imaging (in collaboration with Marcie Glicksman at LDDN) and biochemistry.

Alzheimer disease (AD): We have recently extended our work on stress granules to Alzheimer’s disease. As with ALS, we have shown that tau pathology (neurofibrillary tangles) in the AD brain co-localizes with stress granule markers. The amount of stress granule pathology in the AD brain is very striking. Proteins such as TIA-1, G3BP and TTP, strongly accumulate. Interestingly, though, the pattern of accumulation differs based on the stress granule protein. The pathology appears to correlate with binding to tau protein. TIA-1 and TTP both bind to tau, while G3BP does not bind tau. Stress granules might also directly modulate tau pathology, because co-transfecting TIA-1 with tau induces formation of phosphorylated tau inclusions. The work on AD and stress granules uses biochemical/immunochemical studies focusing on proteins implicated in AD (e.g., antibodies to tau) and on stress granule markers. The work also uses extensive imaging assays (fixed cells, live cell imaging, confocal microscopy). We use studies of hippocampal neurons grown culture, transgenic mice expressing P301L tau and human tissues.

Graduate Faculty (Primary Mentor of Grad Students)
Boston University School of Medicine, Division of Graduate Medical Sciences

Boston University School of Medicine

2017 Boston University: Spivack Award: Distinguished Scholar in Neuroscience
2016 American Association for the Advancement of Science (AAAS): Fellow
2016 New Economy Magazine, World Media Group: Aquinnah Pharmaceuticals Inc., “Most innovative company in neurodegeneration research, 2016”
2013 Alzheimer Association: Zenith Award
2013 Boston University School of Medicine: Evans Center DOM Collaborator of the Year Award: Basic Sciences
2000 Loyola University Dept. of Pharmacology: Faculty of the Year
2000 Loyola University Medical Center: Graduate School Faculty of the Year
1993 Society for Biological Psychiatry: A. E. Bennett Award
1988 Society for Neuroscience: Donald B. Lindsley Prize

Capturing the molecular complexity of Alzheimer's disease through the lens of RNA binding proteins
06/01/2018 - 02/28/2023 (PI)
NIH/National Institute on Aging

RNA binding proteins as novel targets in Alzheimer's disease
09/15/2015 - 04/30/2020 (PI)
NIH/National Institute on Aging

Targeting Stress Granule Biology in Alzheimer's Disease
07/01/2015 - 06/30/2019 (PI)
Bright Focus Foundation

Transformative science driving new treatments for neurodegenerative diseases
02/07/2018 - 02/06/2019 (PI)
Pfizer, Inc.

The Role of Acetylation in regulating pathophysiology of tau
09/01/2014 - 08/31/2018 (PI)
Mayo Clinic NIH NINDS

07/15/2017 - 07/14/2018 (PI)
Cure Alzheimer's Fund

Targeting RNA Metabolism and the Stress Granule Pathway to Inhibit Tau Aggregation
12/31/2015 - 06/30/2018 (PI)
The Edward N. & Della L. Thome Memorial Foundation

It Takes TIA to Tangle: The Role of RNA Binding Proteins in AD
01/01/2014 - 06/30/2017 (PI)
Alzheimer's Association

Regulation of RNA translation by MAPT in Alzheimer's disease
09/01/2015 - 02/28/2017 (PI)
Cure Alzheimer's Fund

Stress Granules and the Biology of TDP-43
01/01/2016 - 12/31/2016 (PI)
NIH/National Institute of Environmental Health Sciences

Showing 10 of 30 results. Show All Results

Yr Title Project-Sub Proj Pubs
2018 Regulation of brain neuroprotection and inflammation by TIA1 1R21AG059925-01
2018 Capturing the molecular complexity of Alzheimer's disease through the lens of RNA binding proteins 1R01AG056318-01A1
2018 TDP-43 aggregation inhibitors for the treatment of ALS 2R44NS095481-03
2018 RNA binding proteins as novel targets in Alzheimer's disease 5R01AG050471-04 2
2017 RNA binding proteins as novel targets in Alzheimer's disease 3R01AG050471-03S1 2
2017 The role of acetylation in regulating pathophysiology of tau 5R01NS089544-04 4
2016 RNA binding proteins as novel targets in Alzheimer's disease 5R01AG050471-02 2
2016 TDP-43 aggregation inhibitors for the treatment of ALS 5R43NS095481-02
2016 The role of acetylation in regulating pathophysiology of tau 5R01NS089544-03 4
2016 Stress Granules and the Biology of TDP-43 4R01ES020395-05 37
Showing 10 of 44 results. Show All Results
Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Faculty can login to make corrections and additions.

  1. Wolozin B. Disrupted in Dementia. Biol Psychiatry. 2018 Oct 01; 84(7):474-475. PMID: 30176990.
  2. Maziuk BF, Apicco DJ, Cruz AL, Jiang L, Ash PEA, da Rocha EL, Zhang C, Yu WH, Leszyk J, Abisambra JF, Li H, Wolozin B. RNA binding proteins co-localize with small tau inclusions in tauopathy. Acta Neuropathol Commun. 2018 Aug 01; 6(1):71.View Related Profiles. PMID: 30068389.
  3. Ruan QT, Yazdani N, Beierle JA, Hixson KM, Hokenson KE, Apicco DJ, Luttik KP, Zheng K, Maziuk BF, Ash PEA, Szumlinski KK, Russek SJ, Wolozin B, Bryant CD. Changes in neuronal immunofluorescence in the C- versus N-terminal domains of hnRNP H following D1 dopamine receptor activation. Neurosci Lett. 2018 Sep 25; 684:109-114.View Related Profiles. PMID: 30003938.
  4. Li D, Wang L, Maziuk BF, Yao X, Wolozin B, Cho YK. Directed evolution of a picomolar-affinity, high-specificity antibody targeting phosphorylated tau. J Biol Chem. 2018 Aug 03; 293(31):12081-12094. PMID: 29899114.
  5. Boeynaems S, Alberti S, Fawzi NL, Mittag T, Polymenidou M, Rousseau F, Schymkowitz J, Shorter J, Wolozin B, Van Den Bosch L, Tompa P, Fuxreiter M. Protein Phase Separation: A New Phase in Cell Biology. Trends Cell Biol. 2018 Jun; 28(6):420-435. PMID: 29602697.
  6. Apicco DJ, Ash PEA, Maziuk B, LeBlang C, Medalla M, Al Abdullatif A, Ferragud A, Botelho E, Ballance HI, Dhawan U, Boudeau S, Cruz AL, Kashy D, Wong A, Goldberg LR, Yazdani N, Zhang C, Ung CY, Tripodis Y, Kanaan NM, Ikezu T, Cottone P, Leszyk J, Li H, Luebke J, Bryant CD, Wolozin B. Reducing the RNA binding protein TIA1 protects against tau-mediated neurodegeneration in vivo. Nat Neurosci. 2018 Jan; 21(1):72-80.View Related Profiles. PMID: 29273772.
  7. Wolozin B, Sotiropoulos I. Dendritic TAU-telidge. EBioMedicine. 2017 06; 20:3-4. PMID: 28529034.
  8. Ash PEA, Stanford EA, Al Abdulatif A, Ramirez-Cardenas A, Ballance HI, Boudeau S, Jeh A, Murithi JM, Tripodis Y, Murphy GJ, Sherr DH, Wolozin B. Dioxins and related environmental contaminants increase TDP-43 levels. Mol Neurodegener. 2017 05 05; 12(1):35.View Related Profiles. PMID: 28476168; DOI: 10.1186/s13024-017-0177-9;.
  9. Russo A, Scardigli R, La Regina F, Murray ME, Romano N, Dickson DW, Wolozin B, Cattaneo A, Ceci M. Increased cytoplasmic TDP-43 reduces global protein synthesis by interacting with RACK1 on polyribosomes. Hum Mol Genet. 2017 Apr 15; 26(8):1407-1418. PMID: 28158562; DOI: 10.1093/hmg/ddx035;.
  10. Maziuk B, Ballance HI, Wolozin B. Dysregulation of RNA Binding Protein Aggregation in Neurodegenerative Disorders. Front Mol Neurosci. 2017; 10:89. PMID: 28420962; DOI: 10.3389/fnmol.2017.00089;.
Showing 10 of 174 results. Show More

This graph shows the total number of publications by year, by first, middle/unknown, or last author.

Bar chart showing 174 publications over 35 distinct years, with a maximum of 10 publications in 1996 and 2001 and 2004 and 2012


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