Rudy Tanzi, Ph.D.
Dr. Rudolph Tanzi serves as Chair of the Cure Alzheimer’s Fund Research Consortium. He is also the Joseph P. and Rose F. Kennedy Professor of Neurology at Harvard University and Director of the Genetics and Aging Research Unit at Massachusetts General Hospital (MGH).
Dr. Tanzi has been a pioneer in genetic studies of neurological disease since the 1980’s when he participated in the first study that to use genetic markers to find a disease gene (Huntington's disease). Dr. Tanzi co-discovered the three familial early-onset Alzheimer's disease (AD) genes and several other neurological disease genes including that responsible for Wilson’s disease. As leader of the Cure Alzheimer’s Fund Alzheimer’s Genome Project, Dr. Tanzi has carried out multiple genome wide association studies of thousands of Alzheimer’s families leading to the identification of over 100 novel AD candidate genes, including CD33. His research on the role of zinc and copper in AD has led to clinical trials of the drug PBT2. Dr. Tanzi serves on dozens of editorial and scientific advisory boards, and has received the two highest awards for Alzheimer's disease research: The Metropolitan Life Award and The Potamkin Prize. He has published over 425 research articles and co-authored the popular trade books “Decoding Darkness” and the recent New York Times Bestseller, “Super Brain”.
Funded Research
Project Description Researchers Funding Alzheimer’s Genome Project™ The goal of this project is to evaluate our new Alzheimer’s disease gene candidates for effects on Alzheimer’s pathology and related biological pathways, including APP processing, amyloid beta protein generation, tangle formation and cell death. These studies are being carried out as part of Phase II of the Alzheimer’s Genome Project (AGP) and entail functional analyses of the Alzheimer’s gene candidates identified in Phase I of the AGP.
Rudy Tanzi, Ph.D. 2005 - 2013
$7,641,000The Amylin Protein of Diabetes Mellitus is an Antimicrobial Peptide The goal of this project is to determine whether the amylin (IAPP) protein has a role in innate immunity (similar to Abeta) in order to significantly advance our understanding of the origins of diabetes pathology and its possible linkage to Alzheimer’s disease.
Robert Moir, Ph.D.Rudy Tanzi, Ph.D.2010 - 2013
$900,000Whole Genome Sequencing We will carry out Whole Genome Sequencing (WGS) of all subjects in the National Institute of Mental Health (NIMH) Alzheimer’s disease family sample (1,510 subjects; 437 AD families). We will identify functional DNA variants throughout the human genome that are inherited as risk factors for Alzheimer’s disease. We also will analyze DNA from brain samples of subjects who exhibited significant Alzheimer’s pathology at autopsy, but never suffered from dementia; this will allow us to identify protective gene variants as well.
Rudy Tanzi, Ph.D. 2012
$750,000Curcumin Collaborative Project This collaborative project will identify and characterize novel curcumin-like derivatives for the treatment and prevention of Alzheimer’s disease. The purpose of the study is to develop means of overcoming obstacles to rapid breakdown and creating methodologies for precisely delivering curcumin derivatives to appropriate locations within the brain.
William Klunk, MD, Ph.D.Rudy Tanzi, Ph.D.2010
$400,000Novel Soluable Gamma-Secretase Modulators Building on in vitro characterization of a novel series of soluable gamma-secretase modulators (SGSMs) funded by Cure Alzheimer’s Fund, the current project is a thorough pharmacological or in vivo examination of these molecules to identify the best or “lead” drug candidate.
Steve Wagner, Ph.D.Rudy Tanzi, Ph.D.2010
$250,000Potential for Host Cytotoxicity from Microbially-derived Abeta Oligomers Alzheimer’s disease (AD) is the most common form of dementia in the elderly afflicting over 20 million people worldwide. Two decades of findings from cell biology, genetic, neuropathological, biochemical and animal studies overwhelmingly point to the β-amyloid peptide (Aβ) as the key protein in the disease’s pathology (see review by Hardy and Selkoe, 20001). Aβ appears to be a soluble component of normal brain. However, in AD brain the peptide accumulates as β-amyloid, an insoluble semi-crystalline deposit that is the hallmark of the disease pathology.
Rudy Tanzi, Ph.D.Robert Moir, Ph.D.Charles Glabe, Ph.D.2009
$250,000Investigation of Certain Properties of Mitochondria Membranes Related to AD While the mechanism of Aβ cytotoxicity remains contentious, evidence is accumulating that membrane permiabilization plays a key role in the pathological activity of the peptide. This study will focus on role of Aβ oligomerization in the Aβ-mediated disruption of lipid bilayers.
Robert Moir, Ph.D.Rudy Tanzi, Ph.D.2008
$200,000Identification of Agents that Inhibit the Generation and Neurotoxicity of Cross-linked B-amyloid Protein Species We have coined the term CAPS to describe cross-linked-Beta-amyloid protein species. CAPS, particularly dimeric forms, are highly neurotoxic. CAPS are also abundant in vivo, with dimeric species alone comprising as much as 40 percent of the total Abeta pool in late state AD brain. In this study we plan to screen compound libraries for potential therapeutic agents that attenuate the levels and/or cytotoxic activity of CAPS.
Robert Moir, Ph.D.Rudy Tanzi, Ph.D.2006 - 2007
$200,000
Selected Publications
These published papers resulted from Cure Alzheimer’s Fund support.
, "The Role of Clusterin, Complement Receptor 1, and Phosphatidylinositol Binding Clathrin Assembly Protein in Alzheimer Disease Risk and Cerebrospinal Fluid Biomarker Levels" , Arch Gen Psychiatry , 68(2) , February 7, 2011 , 207-213, "Age-dependent effect of apolipoprotein E4 on functional outcome after controlled cortical impact in mice" , Journal of Cerebral Blood Flow & Metabolism , 31 , January 2011 , 351–61, "Curcumin Decreases Amyloid-β Peptide Levels by Attenuating the Maturation of Amyloid-β Precursor Protein" , The Journal of Biological Chemistry , 285(37) , Sep 10, 2010 , 28472-80, "Alzheimer's Disease Amyloid-β Links Lens and Brain Pathology in Down Syndrome" , PLoS ONE , 5(5) , May 20, 2010, "Loss-of-Function of ATXN1 Increases Amyloid-Beta Levels by Potentiating Beta-Secretase Processing of APP" , Journal of Biological Chemistry , 285(12) , Mar 19, 2010 , 8515-26, "Protein Aggregates and Novel Presenilin Gene Variants in Idiopathic Dilated Cardiomyopathy" , Circulation: Journal of the American Heart Association , 121(10) , Mar 16, 2010 , 1216-26, "Familial Alzheimer's Disease Mutations in Presenilin 1 Do Not Alter Levels of the Secretase Amyloid-Beta Protein Precursor Generated by Beta-Secretase Cleavage" , Current Alzheimer Research , 7(1) , February 2010 , 21-6, "CALHM1 P86L polymorphism does not alter amyloid-β or tau in cerebrospinal fluid" , Neuroscience Letters , Volume 469, Issue 2 , Jan 22 2010 , 265-267, "Maximizing the Power of Genome-Wide Association Studies: A Novel Class of Powerful Family - Based Association Tests" , Statistics in Biosciences , 1(2) , Nov 2009 , 125-143
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