Explore This Lab


Since 1982, Dr. Tanzi has focused his studies on Alzheimer's disease (AD). He isolated the first familial Alzheimer's disease (FAD) gene, known as the amyloid beta-protein (A4) precursor (APP) in 1987, and another in 1995, called presenilin 2. He also collaborated on the isolation of the second FAD gene, presenilin 1.

In 1993, Dr. Tanzi isolated the gene responsible for the neurological disorder known as Wilson's disease, and over the past 25 years, he has collaborated on studies identifying several other neurodegenerative disease genes including those causing amyotrophic lateral sclerosis and neurofibromatosis.

Dr. Tanzi’s laboratory first discovered that the metals zinc and copper are necessary for the formation of neurotoxic assemblies of the AD-associated peptide, A-beta, the main component of beta-amyloid deposits in brains of AD patients. These studies have led to ongoing clinical trials for treating and preventing AD by targeting A-beta metal interactions. Dr. Tanzi was also involved in the first studies implicating gamma-secretase modulators as therapeutics for AD.

Dr. Tanzi is currently carrying out genome wide association screens to identify novel genes associated with AD and autism spectrum disorders. Candidate disease genes are then characterized at the molecular, cell biological, and biochemical levels to elucidate disease mechanisms.

Research Projects

A study from the Tanzi Lab and collaborators suggests that A-beta is a hitherto unrecognized antimicrobial peptide (AMP) that may normally function in the innate immune system. This finding stands in stark contrast to current models of A-beta-mediated pathology and has important implications for ongoing and future AD treatment strategies.

low magnification electron micrograph
A low magnification electron micrograph of the same experiment shows the result of A-beta added to bacteria (left side), compared with the right side, with no A-beta.

We have shown that A-beta is active against at least eight common and clinically relevant microorganisms. This photomicrograph (18,500x) shows bacteria being attacked by A-beta, which is forming beta-amyloid fibrils and attaching to other the bacteria in the picture. The fibrils eventually entrap the bacteria and cause them to lyse.

Study co-authors: Lee Goldstein, MD; Robert Moir, PhD; Rudy Tanzi, PhD

About Dr. Tanzi

Dr. Rudolph Tanzi is the Director of the Genetics and Aging Research Unit, Co-Director of the McCance Center for Brain Health, Co-Director of the MassGeneral Institute for Neurodegenerative Disease, and Vice-Chair of Neurology (Research), at Massachusetts General Hospital, and the Joseph P. and Rose F. Kennedy Professor of Neurology at Harvard Medical School. Dr. Tanzi co-discovered the first three Alzheimer’s disease genes, including APP and directs the Cure Alzheimer’s Fund Alzheimer’s Genome Project, which identified the first neuroinflammation-related Alzheimer’s gene, CD33. He has also been developing therapies for treating and preventing AD using 3D human neural glial culture models of AD and is now testing them in various clinical trials. Dr. Tanzi has published over 600 papers, received numerous awards, including the Metropolitan Life Award, Potamkin Prize, Smithsonian American Ingenuity Award, and was one of the TIME100 Most Influential People in the World. Dr. Tanzi is a New York Times bestselling author, and co-authored “Decoding Darkness,” “Super Brain”, “Super Genes”, and “The Healing Self.” He has also hosted three PBS shows and made numerous appearances on network and cable news and medical television shows. In his spare time, he plays keyboards for Joe Perry, Aerosmith and other musicians.