Li-Huei Tsai, Ph.D.

Director, The Picower Institute for Learning and Memory

Lead Investigator, MIT’s Aging Brain Initiative

Picower Professor of Neuroscience, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology

Associate Director of the Glenn Labs for Aging Research at MIT

Associate Member, Broad Institute

Professor Tsai is a leader in understanding the molecular pathophysiology of neurological disorders affecting cognition. Her work has brought new mechanisms for learning, memory and neurodegeneration to light and suggests new paths for combatting age-related memory loss.

Landmark discoveries include pinpointing major genetic risk for Alzheimer’s disease to immune genes, identifying chromatin-modifiers and kinases that regulate brain flexibility and can be targeted to improve cognition in Alzheimer’s disease, and discovering that genomic integrity is critical for neuronal protection during both aging and neurodegenerative disease.

Dr. Tsai is a recipient of the Young Investigator Award, Metropolitan Life Foundation, Outstanding Contributor Award of the Alzheimer Research Forum, the NIH Cantoni Lecture Award and the Glenn Award For Research in Biological Mechanisms of Aging.

She is a Fellow of the American Association for the Advancement of Science and a member of the Institute of Medicine of the National Academy of Sciences, the Neurodegeneration Consortium and Taiwan’s Academia Sinica.

Dr. Tsai has authored and co-authored over 130 peer-reviewed articles published in Nature, Cell, Neuron, Molecular Psychiatry, The Journal of Neuroscience, Nature Neuroscience, and the Proceedings of the National Academy of Sciences.  Her research has been featured in National Geographic and the Boston Globe.

 

Funded Research

Project Description Researchers Funding
CIRCUITS: Production Center for Reference and Variation Gene-Regulatory Maps

Alzheimer’s disease is a devastating neurodegenerative disorder, afflicting 1 in 3 dying seniors and costing $236 billion annually in the United States alone. Its prevalence is increasing rapidly in an aging population, and currently there is no cure. Recent genetic studies provide new hope for therapeutic avenues, but translating genetic results into therapeutics has been remarkably difficult, due primarily to the fact that most genetic mutations do not alter protein function directly, but instead affect the expression of nearby genes in subtle ways.

2016
$750,000
Studying the Functional Consequences of Alzheimer’s Disease Risk Variants in the CLU and ABCA7 Genes Using Both Human and Mouse Models

The vast majority of people with Alzheimer’s disease (AD) suffer from the sporadic (late-onset) form, whose causes remain completely unknown. From studies involving thousands of people, researchers have identified a number of genetic variants that may increase one’s risk for sporadic AD (sAD). However, little is understood regarding how carrying these variants impacts one’s sAD risk.

2015 to 2016

$500,000
CIRCUITS: Functional Analysis of Alzheimer’s Disease Risk Genes Using Human-Induced Pluripotent Stem Cells

The vast majority of people with Alzheimer’s disease (AD) suffer from the sporadic, or late-onset form, which causes remain completely unknown. From studies involving thousands of people, researchers have identified a number of genetic variants that may increase one’s risk for sporadic AD. However, little is understood regarding why these small changes impact one’s risk to develop AD. In this work, we will use the cutting-edge genome editing technique CRISPR/Cas9 to introduce AD-associated genetic variants identified through genome-wide analysis into reprogrammed human stem cells.

2016
$400,000

Selected Publications

These published papers resulted from Cure Alzheimer’s Fund support.
Rebecca G. Canter, Jay Penney, and Li-Huei Tsai, The road to restoring neural circuits for the treatment of Alzheimer's disease, Nature, 539(7628), 10 Nov 2016, 187–196