Rudolph E. Tanzi Quotes

Rudolph Tanzi is the Joseph P. and Rose F. Kennedy Professor of Neurology at Harvard University, and Vice-Chair of Neurology, Director of the Genetics and Aging Research Unit, and Co-Director of the Henry and Allison McCance Center for Brain Health at Massachusetts General Hospital . Tanzi has been investigating the genetics of neurological disease since a student in the 1980s when he participated in the first study that used genetic markers to find a disease gene . Tanzi co-discovered all three familial early-onset Alzheimer's disease genes and several other neurological disease genes including that responsible for Wilson’s disease. As the leader of the Cure Alzheimer's Fund Alzheimer’s Genome Project, Tanzi has carried out multiple genome wide association studies of thousands of Alzheimer’s families leading to the identification of novel AD candidate genes, including CD33 and the first two rare mutations causing late-onset AD in the ADAM10 gene. His research on the role of zinc and copper in AD has led to clinical trials at Prana Biotechnology. He is also working on gamma secretase modulators for the prevention and treatment of Alzheimer's. He also serves as Chair of the Cure Alzheimer's Fund Research Leadership Group and Director the Cure Alzheimer’s Fund Alzheimer’s Genome Project™.

Dr. Tanzi and his team have used Alzheimer’s genes and human stem cells to create “Alzheimer’s-in-a-Dish” - a three-dimensional human stem cell-derived neural culture system that was the first to recapitulate both pathological hallmarks of Alzheimer’s disease: plaques and tangles. This model has made drug screening for Alzheimer’s disease considerably faster and more effective. Using this system, Dr. Tanzi has developed several novel therapies for AD including gamma secretase modulators aimed at plaque pathology. These promising drugs are now heading into clinical trials in Alzheimer’s disease. Most recently, Dr. Tanzi and his team have discovered that beta-amyloid, the main component of senile plaques, may play a role in the innate immune system of the brain operating as an anti-microbial peptide, suggesting a possible role for infection in the etiology and pathogenesis of AD. Most recently, Dr. Tanzi showed a link between herpes viruses and plaque production in Alzheimer's disease, proposing the hypothesis that brain plaques causing Alzheimer's disease may form as a defense mechanism to protect the brain against viruses, bacteria and other microbes. Wikipedia

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