Rudy Tanzi, Ph.D.

Dr. Rudolph Tanzi is the Vice-Chair of Neurology and Director of the Genetics and Aging Research Unit at Massachusetts General Hospital, and serves as the Joseph P. and Rose F. Kennedy Professor of Neurology at Harvard Medical School. 

Dr. Tanzi co-discovered three of the first Alzheimer’s disease genes and has identified several others in the Alzheimer’s Genome Project, which he directs. He also discovered the Wilson’s disease gene and participated in the discovery of several other neurological disease genes. Most recently, he has used AD genes to create a three- dimensional human stem cell-derived neural culture system that recapitulates AD plaque and tangle pathology. Using this system, Dr. Tanzi is also developing therapeutics for AD including gamma secretase modulators and metal chaperones to lower beta-amyloid and tangle burden in the brain.

Dr. Tanzi has published nearly 500 research papers and has received the highest awards in his field, including the Metropolitan Life Foundation Award and Potamkin Prize. Most recently, he received the 2015 Smithsonian American Ingenuity Award and was named to the 2015 list of TIME100 Most Influential People in the World.

He co-authored the popular trade books “Decoding Darkness”, New York Times Bestseller, “Super Brain”, and “Super Genes” He was named by GQ magazine as a Rock Star of Science, and in his spare time, has played keyboards with the band Aerosmith, guitarist, Joe Perry, and singer, Chris Mann.

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.

2005 to 2016

Microglial Core/CD33 and Alzheimer’s Disease: From Biology to Therapy

Our current inability to prevent or delay Alzheimer’s disease (AD) and the expected increase in the prevalence of AD are predicted to give rise to a global AD pandemic. We recently have identified a novel pathway for amyloid beta (Abeta) clearance in the aging brain that is highly relevant to AD pathogenesis. In a very large family-based, genome-wide association study, we identified CD33 as a novel late-onset AD risk factor. CD33 encodes a transmembrane sialic acid-binding immunoglobulin-like lectin that regulates innate immunity.

2015 to 2016

Search for Female-Specific Genetic Factors Contributing to Risk for Alzheimer’s Disease

This multidimensional investigation will seek to elucidate sex-linked factors that determine Alzheimer’s disease risk, age of onset and rate of progression, powerful information that would contribute to the pursuit of a cure for both sexes. Women make up more than two-thirds of the Alzheimer’s patient population, yet very little is known or understood about why this is the case or what it means about the disease’s mechanisms of action, risk factors and progression.

Role of Neurexins in Alzheimer’s Disease Pathophysiology

Pathogenesis of Alzheimer's disease (AD) is directly linked to levels of the toxic amyloid beta (Abeta) peptide in the brain. Abeta levels and amyloid deposition increase in aging and in AD, yet age-dependent factors that increase Abeta levels at the synapse remain largely unknown. In large family-based genome-wide association studies (GWAS), we recently have discovered a strong association between a neurexin gene and late-onset AD, and identified a number of neurexin variants that are associated with increased risk for AD.

Lead Optimization and Lead Evolution of Potent SGSMs for the Treatment of Alzheimer’s Disease

This application outlines a highly focused extension of an NIH-funded Blueprint Neurotherapeutics (BPN) U01 program to create more potent, soluble, brain penetrant, nontoxic small molecules known as soluble gamma-secretase modulators (SGSMs) that act to enhance the activity/processivity of y-secretase, thereby reducing the levels of Aβ42 and to a lesser extent Aβ40 while increasing the levels of shorter Abeta peptides (e.g., Aβ38 and Aβ37)

Whole 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.

2012 to 2014

The 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.

2010 to 2014

Generation of Neural Progenitor Cells Overexpressing Alzheimer’s Disease Genes with Familial Mutations and Analysis of Pathological Changes of Alzheimer’s Cells in Vivo

We seek to evaluate the impact of candidate AD drugs on Abeta and tau pathology in human cellular AD models. In collaboration with Dr. Tanzi’s laboratory (Massachusetts General Hospital), we will test the impact of select candidate AD drugs on both Abeta and tau pathology in the 30 human neural cell culture models developed in Aim 4. In the first year, we found that SGSM41i, a candidate AD drug designed to specifically decrease the toxic Abeta42 generation, decreases not only the Abeta plaques but also the tau pathology in the 30 human cellular AD models.

Curcumin 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.

Novel 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.

Potential 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.

Oligomer Collaborative Projects

A collaboration of members of the Research Consortium, a member of the Cure Alzheimer’s Fund Science Advisory Board and non-Cure Alzheimer’s Fund-affiliated researchers hypothesizes that an abnormal increase in levels of synaptic Abeta and, particularly, Abeta oligomers may lead to synaptic dysfunction, cognitive decline and eventually dementia. This highly innovative collaborative project will address how Abeta oligomers are formed and which types detrimentally impact synaptic dysfunction and neuronal survival in the brain.

2006 to 2008

Investigation 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.

Identification 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.

2006 to 2007


Selected Publications

These published papers resulted from Cure Alzheimer’s Fund support.
Myles R. Minter, Reinhard Hinterleitner, Marlies Meisel, Can Zhang, Vanessa Leone, Xiaoqiong Zhang, Paul Oyler-Castrillo, Xulun Zhang, Mark W. Musch, Xunuo Shen, Bana Jabri, Eugene B. Change, Rudolph E. Tanzi, Sangram Sisodia, Antibiotic-induced perturbations in microbial diversity during post-natal development alters amyloid pathology in an aged APP(SWE)/PS1(Delta E9) murine model of Alzheimer's disease, Scientific Reports, 7, 5 Sep 2017
Dragan Gamberger, Nada Lavrač, Shantanu Srivatsa, Rudolph E. Tanzi, P. Murali Doraiswamy, Identification of clusters of rapid and slow decliners among subjects at risk for Alzheimer's disease, Scientific Reports, 7, 28 Jul 2017
Feng Liang, Yu Wan, Diane Schaak, Joseph Ward, Xunuo Shen, Rudolph E. Tanzi, Can Zhang, Qimin Quan, Nanoplasmonic fiber tip probe detects significant reduction of intracellular Alzheimer's diseaserelated oligomers by curcumin, Scientific Reports, 7, 18 Jul 2017
Wilbur Song, Basavaraj Hooli, Kristina Mullin, Sheng Chih Jin, Marina Cella, Tyler K. Ulland, Yaming Wang, Rudolph E. Tanzi, Marco Colonna, Alzheimer's disease-associated TREM2 variants exhibit either decreased or increased ligand-dependent activation, Alzheimer's & Dementia, 13(4), Apr 2017, 381–387
Heide Loehlein Fier, Dmitry Prokopenko, Julian Hecker, Michael H. Cho, Edwin K. Silverman, Scott T. Weiss, Rudolph E. Tanzi, Christoph Lange, On the association analysis of genome-sequencing data: A spatial clustering approach for partitioning the entire genome into nonoverlapping windows, Genetic Epidemiology, 41(4), 20 Mar 2017, 332–340
Deepak Kumar Vijaya Kumar , William A Eimer , Rudolph E Tanzi and Robert D Moir, Alzheimer’s disease: the potential therapeutic role of the natural antibiotic amyloid-β peptide, Neurodegenerative Disease Management, 6(5), 7 Sep 2016, 345–348
Wilbur Song, Basavaraj Hooli, Kristina Mullin, Sheng Chih Jin, Marina Cella, Tyler K. Ulland, Yaming Wang, Rudolph Tanzi, Marco Colonna, Alzheimer's disease-associated TREM2 variants exhibit either decreased or increased ligand-dependent activation, Alzheimer's & Dementia, 9 Aug 2016
C Herold, B V Hooli, K Mullin, T Liu, J T Roehr, M Mattheisen, A R Parrado, L Bertram, C Lange and R E Tanzi, Family-based association analyses of imputed genotypes reveal genome-wide significant association of Alzheimer’s disease with OSBPL6, PTPRG, and PDCL3, Molecular Psychiatry, February 2016
Carla D'Avanzo, Jenna Aronson, Young Hye Kim, Se Hoon Choi, Rudolph E. Tanzi and Doo Yeon Kim, Alzheimer's in 3D culture: Challenges and perspectives, BioEssays, 37(10), October 2015, 1139–1148
Young Hye Kim, Se Hoon Choi, Carla D'Avanzo, Matthias Hebisch, Christopher Sliwinski, Enjana Bylykbashi, Kevin J Washicosky, Justin B Klee, Oliver Brüstle, Rudolph E Tanzi & Doo Yeon Kim, A 3D human neural cell culture system for modeling Alzheimer’s disease, Nature Protocols, 10(7), June 2015, 985–1006
Carla D’Avanzo, Christopher Sliwinski, Steven L. Wagner, Rudolph E. Tanzi, Doo Yeon Kim, and Dora M. Kovacs, γ-Secretase modulators reduce endogenous amyloid β42 levels in human neural progenitor cells without altering neuronal differentiation, The FASEB Journal, 29(8), 22 April 2015, 3335-3341
Karthikeyan Veeraraghavalu, Can Zhang, Xiaoqiong Zhang, Rudolph E. Tanzi, and Sangram S. Sisodia, Age-Dependent, Non-Cell-Autonomous Deposition of Amyloid from Synthesis of β-Amyloid by Cells Other Than Excitatory Neurons, J Neurosci, 34(10), 5 March 2014, 3668-3673
Xu Z, Dong Y, Wang H, Culley DJ, Marcantonio ER, Crosby G, Tanzi RE, Zhang Y, Xie Z, Age-dependent postoperative cognitive impairment and Alzheimer-related neuropathology in mice, Sci Rep, 4, January 20, 2014, 3766
Jaehong Suh, Se Hoon Choi, Donna M. Romano, Moira A. Gannon, Andrea N. Lesinski, Doo Yeon Kim, Rudolph E. Tanzi, ADAM10 Missense Mutations Potentiate β-Amyloid Accumulation by Impairing Prodomain Chaperone Function, Neuron, 80(2), Oct 16, 2013, 385–401
Li A, Ahsen OO, Liu JJ, Du C, McKee ML, Yang Y, Wasco W, Newton-Cheh CH, O'Donnell CJ, Fujimoto JG, Zhou C, Tanzi RE, Silencing of the Drosophila ortholog of SOX5 in heart leads to cardiac dysfunction as detected by optical coherence tomography, Hum Mol Genet, 22(18), September 15, 2013, 3798-3806
Rudolph E Tanzi, Decoding Alzheimer's in the age of genome-wide analyses, Mol Neurodegener, 8(suppl 1), September 13. 2013, 01
BV Hooli1, ZM Kovacs-Vajna2, K Mullin1, MA Blumenthal1, M Mattheisen3, C Zhang1, C Lange4, G Mohapatra5, L Bertram6 and RE Tanzi1, Rare autosomal copy number variations in early-onset familial Alzheimer’s disease, Molecular Psychology, 6/11/2013
Zhongcong Xie, MD, PhD, Sayre McAuliffe, Celeste A. Swain, Sarah A. P. Ward, Catherine A. Crosby, Hui Zheng, Janet Sherman, Yuanlin Dong, Yiying Zhang, Neelakantan Sunder, Dennis Burke, Kevin Washicosky, Rudolph E. Tanzi, and Edward R. Marcantonio, Cerebrospinal Fluid Aβ to Tau Ratio and Postoperative Cognitive Change, Annals of Surgery, Ann Surg 2013;00 , 5/10/2013, 1-6
Wagner SL, Tanzi RE, Mobley WC, Galasko D, Potential Use of γ-Secretase Modulators in the Treatment of Alzheimer Disease, Arch Neurol., July 16, 2012
Wu X, Lu Y, Dong Y, Zhang G, Zhang Y, Xu Z, Culley DJ, Crosby G, Marcantonio ER, Tanzi RE, Xie Z, The inhalation anesthetic isoflurane increases levels of proinflammatory TNF-α, IL-6, and IL-1β, Neurobiology of Aging, 33(7), July 2012, 1364-78
B.V. Hooli, PhD, G. Mohapatra, PhD, M. Mattheisen, MD, A.R. Parrado, PhD, J.T. Roehr, MS, Y. Shen, PhD, J.F. Gusella, PhD, R. Moir, PhD, A.J. Saunders, PhD, C. Lange, PhD, R.E. Tanzi, PhD and L. Bertram, MD, Role of common and rare APP DNA sequence variants in Alzheimer disease, Neurology 78 , 78/16, April 17, 2012, 1250-1257
Xie Z, Dong Y, Maeda U, Xia W, Tanzi RE, RNAi-mediated knock-down of Dab and Numb attenuate Aβ levels via γ-secretase mediated APP processing, Transl Neurodegener., 1:8, Mar 22, 2012
Lill CM, Roehr JT, McQueen MB, Kavvoura FK, Bagade S, Schjeide BM, Schjeide LM, Meissner E, Zauft U, Allen NC, Liu T, Schilling M, Anderson KJ, Beecham G, Berg D, Biernacka JM, Brice A, DeStefano AL, Do CB, Eriksson N, Factor SA, Farrer MJ, Foroud T, Gasser T, Hamza T, Hardy JA, Heutink P, Hill-Burns EM, Klein C, Latourelle JC, Maraganore DM, Martin ER, Martinez M, Myers RH, Nalls MA, Pankratz N, Payami H, Satake W, Scott WK, Sharma M, Singleton AB, Stefansson K, Toda T, Tung JY, Vance J, Wood NW, Zabetian CP; 23andMe Genetic Epidemiology of Parkinson's Disease Consortium; International Parkinson's Disease Genomics Consortium; Parkinson's Disease GWAS Consortium; Wellcome Trust Case Control Consortium 2), Young P, Tanzi RE, Khoury MJ, Zipp F, Lehrach H, Ioannidis JP, Bertram L, Comprehensive research synopsis and systematic meta-analyses in Parkinson’s disease genetics: The PDGene database, PLoS Genet., 8(3), March 2012, e1002548
Yiying Zhang MD, MS1, Zhipeng Xu MD, PhD1, Hui Wang MD1,2, Yuanlin Dong MD, MS1, Hai Ning Shi PhD, DVM3, Deborah J. Culley MD4, Gregory Crosby MD4, Edward R. Marcantonio MD5, Rudolph E. Tanzi PhD.6, Zhongcong Xie MD, PhD1,*, Anesthetics Isoflurane and Desflurane Differently Affect Mitochondrial Function, Learning, and Memory, Annals of Neurology, Volume 71, Issue 5, February 24, 2012, 687–698
Sungho Wona, Qing Luc, Lars Bertram, Rudolph E. Tanzi, Christoph Lange, On the Meta-Analysis of Genome-Wide Association Studies: A Robust and Efficient Approach to Combine Population and Family-Based Studies, Human Heredity , 73, January 18, 2012, 35-46
Sarajärvi T, Tuusa JT, Haapasalo A, Lackman JJ, Sormunen R, Helisalmi S, Roehr JT, Parrado AR, Mäkinen P, Bertram L, Soininen H, Tanzi RE, Petäjä-Repo UE, Hiltunen M, Cysteine 27 Variant of the δ-Opioid Receptor Affects Amyloid Precursor Protein Processing through Altered Endocytic Trafficking, Mol Cell Biol., 31(11), June 2011, 2326–2340
A. Li, C. Zhou, J. Moore, P. Zhang, T.-H. Tsai, H.-C. Lee, D.M. Romano, M.L. McKee, D.A. Schoenfeld, M.J. Serra,3 K. Raygor, H.F. Cantiello, J.G. Fujimoto, and R.E. Tanzi, Changes in the Expression of the Alzheimer’s Disease- Associated Presenilin Gene in Drosophila Heart Leads to Cardiac Dysfunction, NIHPA Author Manuscripts , 8/3, May 1, 2011, 313-322
Viswanathan J, Haapasalo A, Bottcher C, Miettinen R, Kurkinen KMA, Lu A, Thomas A, Maynard CJ, Romano D, Hyman BT, Berezovska O, Nertram L, Soininen H, Dantuma NP, Tanzi RE, Hiltunen M, Alzheimer's Disease-Associated Ubiquilin-1 Regulates Presenilin-1 Accumulation and Aggresome Formation, Traffic, 12(3), Mar 12, 2011, 330-48
Brit-Maren M. Schjeide, BS; Cathrin Schnack, PhD; Jean-Charles Lambert, PhD; Christina M. Lill, MD; Julia Kirchheiner, MD, PhD; Hayrettin Tumani, MD; Markus Otto, MD; Rudolph E. Tanzi, PhD; Hans Lehrach, PhD; Philippe Amouyel, PhD; Christine A. F. von Arnim, MD; Lars Bertram, MD, 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
Mannix RC, Zhang J, Park J, Zhang X, Bilal K, Walker K, Tanzi RE, Tesco G, Whalen MJ, 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
Bertram L, Lill CM, Tanzi RE, The Genetics of Alzheimer Disease: Back to the Future, Neuron, 68(2), Oct 21, 2010, 270-81
Zhang C, Browne A, Child D, Tanzi RE, 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
Moncaster JA, Pineda R, Moir RD, Lu S, Burton MA, Ghosh JG, Ericsson M, Soscia SJ, Mocofanescu A, Folkerth RD, Robb RM, Kuszak JR, Clark JI, Tanzi RE, Hunter DG, Goldstein LE, Alzheimer's Disease Amyloid-β Links Lens and Brain Pathology in Down Syndrome, PLoS ONE, 5(5), May 20, 2010
Zhang C, Browne A, Child D, DiVito JR, Stevenson JA, Tanzi RE, 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
Gianni D, Li A, Tesco G, McKay KM, Moore J, Raygor K, Rota M, Gwathmey JK, Dec GW, Aretz T, Leri A, Semigran MJ, Anversa P, Macgillivray TE, Tanzi RE, delMonte F., 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
Giedraitis V, Glaser A, Sarajarvi T, Brundin R, Gunnarsson MD, Schjeide B-M, Tanzi RE, Helisalmi S, Pirttila T, Kilander L, Lannfelt L, Soininen H, Bertram L, Ingelsson M, Hiltunen M, CALHM1 P86L polymorphism does not alter amyloid-β or tau in cerebrospinal fluid, Neuroscience Letters, Volume 469, Issue 2, Jan 22 2010, 265-267
Won S, Bertram L, Becker D, Tanzi RE, Lange C., 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
Bertram, L, Tanzi RE, Genome-wide association studies in Alzheimer's disease, Human Molecular Genetics, Vol 18, Review Issue 2, Oct 15, 2009
Kim M, Suh J, Romano D, Truong MH, Mullin K, Hooli B, Norton D, Tesco G, Elliot K, Wagner SL, Moir RD, Becker KD, Tanzi RE., Potential late-onset Alzheimer's disease-associated mutations in the ADAM10 gene attenuate alpha-secretase activity., Human Molecular Genetics, Vol 18, Oct 15, 2009
Hooli BV, Tanzi RE, A current view of Alzheimer's disease, F1000 Biology Rep., 1, July 8, 2009, 54
Dong Y, Zhang G, Zhang B, Moir RD, Xia W, Marcantonio ER, Culley DJ, Crosby G, Tanzi RE, Xie Z, The Common Inhalational Anesthetic Sevoflurane Induces Apoptosis and Increases β-Amyloid Protein Levels, Archives of Neurology, Vol. 66 No. 5, May 2009
Schjeide BM, McQueen MB, Mullin K, DiVito J, Hogan MF, Parkinson M, Hooli B, Lange C, Blacker D, Tanzi RE, and Bertram L., Assessment of Alzheimer's disease case-control associations using family-based methods, Neurogenetics, DOI 10.1007/s10048-008-1051-3,, Feb 10, 2009, 568-580
Schjeide BM, Hooli B, Parkinson M, Hogan MF, DiVito J, Mullin K, Blacker D, Tanzi RE, Bertram L, GAB2 as an Alzheimer Disease Susceptibility Gene, Follow up of Genomewide Association Results, Arch Neurol, 66, Feb 2009, 250 – 254
Bertram L, Schjeide BM, Hooli B, Mullin K, Hiltunen M, Soininen H, Ingelsson M, Lannfelt L, Blacker D, Tanzi RE., No association between CALHM1 and Alzheimer's disease risk., Cell, 135(6), Dec 12 2008, 993-4
Xie Z, Culley DJ, Dong Y, Zhang G, Zhang B, Moir RD, Frosch MP, Crosby G, Tanzi RE. , The common inhalation anesthetic isoflurane induces caspase activation and increases Aβ level in vivo., Annals of Neurology, Volume 64, Dec 2008
Cotton RG, Auerbach AD, Axton M, Barash CI, Berkovic SF, Brookes AJ, Burn J, Cutting G, den Dunnen JT, Flicek P, Freimer N, Greenblatt MS, Howard HJ, Katz M, Macrae FA, Maglott D, Möslein G, Povey S, Ramesar RS, Richards CS, Seminara D, Smith TD, Sobrido MJ, Solbakk JH, Tanzi RE, Tavtigian SV, Taylor GR, Utsunomiya J, Watson M, The Human Variome Project, Science., 322(5903), Nov 7 2008, 861-2
Bertram L, Lange CL, Mullin K, Parkinson M, Hsiao M, Hogan MF,  Schjeide BMM, Hooli B, DeVito J, Ionita I, Jiang H, Laird N, Moscarillo T, Ohlsen KL, Elliott K, Wang X, Hu-Lince D, Ryder M, Murphy A, Wagner SL, Blacker D, Becker KD, Tanzi RE., Genome-wide Association Analysis Reveals Putative Alzheimer's Disease Susceptibility Loci in Addition to APOE, Am. J. Hum. Genet., 83, November 2008, 623-632
Bertram L, Tanzi RE, Thirty years of Alzheimer’s disease genetics: the implications of systematic meta-analyses, Nature Reviews Neurosci., October 2008
Schaffer B, Bertram L, Miller L, Mullin K, Weintraub S, Johnson N, Bigio E, Mesulam M, Wiedau-Pazos M, Jackson G, Cummings J, Cantor R, Levey A, Tanzi RE, and Geschwind D, Association of GSK3B with Alzheimer's Disease and Frontotemporal Dementia, Arch. Neurol., 65(10), October 2008, 1368-1374
Zhang B, Dong Y, Zhang G, Moir RD, Xia W, Yue Y, Tian M, Culley DJ, Crosby G, Tanzi RE, Xie Z, The inhalation anesthetic desflurane induces caspase activation and increases amyloid-beta protein levels under hypoxic conditions., J Biol Chem., 2;283(18), May 2, 2008, 11866-75
Zhang G, Dong Y, Zhang B, Ichinose F, Wu X, Culley DJ, Crosby G, Tanzi RE, Xie Z., Isoflurane-induced caspase-3 activation is dependent on cytosolic calcium and can be attenuated by memantine., J Neurosci, 28, April 23, 2008, 4551-60
Tesco G, Koh YH, Kang E, Cameron A, Das S, Sena-Esteves M, Hiltunen, Yang S-H, Zhong Z, Shen Y, Simpkins J, Tanzi RE., Depletion of GGA3 stabilizes BACE and enhances β-secretase activity, Neuron, 54(5), 2007, 721-37
Kim M, Hersh LB, Leissring MA, Ingelsson M, Matsui T, Farris W, Lu A, Hyman BT, Selkoe DJ, Bertram L, Tanzi RE, Decreased catalytic activity of the insulin degrading enzyme in chromosome 10-linked Alzheimer’s disease families., Journal of Biological Chemistry, 282(11), 2007, 7825-32
Xie Z, Dong Y, Maeda U, Moir R, Xia W, Culley DJ, Crosby G, Tanzi RE., The Inhalation Anaesthetic Isoflurane Induces a Vicious Cycle of Apoptosis and Aβ Accumulation., J. Neurosci., 27, 2007, 1247-1254
McQueen MB, Bertram L, Lange C, Becker KD, Albert MS, Tanzi RE, Blacker D., Exploring Candidate Gene Associations with Neuropsychological Performance., Am J Med Genet B Neuropsychiatr Genet, 144(8), 2007, 987-91