Posts by Rudolph E. Tanzi, PhD
How Amyloid-beta Forms Suggests New Strategies for Preventing, Treating Alzheimer's Disease
In a study with major implications for drug development in Alzheimer's disease, Raja Bhattacharyya, PhD, and Rudolph E. Tanzi, PhD, of the McCance Center for Brain Health, and colleagues have determined how neurotoxic amyloid-β is generated in axons and how its production can be reduced.
Whole-Genome Sequencing Suggests New Approaches to Drug Development for Alzheimer's Disease
Dmitry Prokopenko, PhD, and Rudolph E. Tanzi, PhD, of the Department of Neurology, and colleagues have completed the first systematic whole-genome sequencing study in Alzheimer's disease (AD), detecting 13 rare gene variants not previously associated with AD and linked to neuroplasticity and loss of synapses.
The Innate Immune Protection Hypothesis of Alzheimer's Disease
Alzheimer's disease research at Massachusetts General Hospital has led to a new immune protection hypothesis that may lead to new treatment and prevention options.
Cromolyn Sodium Provides Neuroprotection in Animal Model of ALS
Building on similar research in Alzheimer's disease, researchers at Massachusetts General Hospital demonstrated that treatment with cromolyn sodium delayed disease onset and was neuroprotective in a mouse model of amyotrophic lateral sclerosis by decreasing the inflammatory response.
New Model Allows Screening of Drugs to Improve Blood–Brain Barrier Integrity in Alzheimer's Disease
A new in vitro model of Alzheimer's disease will facilitate studies of blood–brain barrier (BBB) dysfunction, studies of the mechanisms by which BBB impairment affects the pathogenesis of the disease and screening of drugs to improve BBB function.
"Crosstalk" Between Genes Promotes Brain Inflammation in Alzheimer's Disease
A new study reveals that genes CD33 and TREM2 interact to manage the inflammation of amyloid plaque, making them ideal drug targets for the prevention of brain nerve cell death prior to development of Alzheimer's disease.
Unconventionality in Alzheimer's Research and the Pursuit of Validation
From the 1980s, scientists understood beta-amyloid were a toxic byproduct that, when deposited in the brain, caused Alzheimer's. However, Dr. Robert Moir followed an unconventional research path, and revealed that the development of amyloid plaques might be an immune response to microbe infections.
Study Suggests Exercise May Boost Brain Power in Alzheimer's
An animal study from researchers at Massachusetts General Hospital showed the effects of exercise on promoting neurogenesis, the growth of new brain cells.
Brain Infection with Herpes Virus May Accelerate Progression of Alzheimer's Disease
Laboratory studies at Mass General suggest that active herpes infections in the brain may accelerate amyloid deposition and the progression of Alzheimer's disease.
Alzheimer’s in a Dish Model Replicates Pathology, Including Inflammation
A Mass General research team has built on their previous development of a system that fully replicates the pathology behind Alzheimer’s disease to now include inflammation
The focus of Dr. Tanzi's research is in identifying and characterizing the genetic and environmental factors involved in neurodegeneration in Alzheimer's disease in autism. In addition to identifying risk factors for Alzheimer's disease, he and his colleagues address the mechanisms underlying the etiology and pathogenicity of the genes responsible for Alzheimer's disease through the application of molecular, cell biological, and biochemical strategies.
Dr. Tanzi's ongoing research in AD and autism follows a basic roadmap, which includes disease gene discovery, translational and functional studies to identify pathogenic gene variants and mutations, molecular biological and biochemical studies to elucidate pathways that have been impacted by disease-associated gene changes, and novel drug screening assays to identify small molecules or supplements that can halt or reverse pathogenic molecular and biochemical phenotypes at the cellular level.