Li-Huei Tsai is an American neuroscientist and the director of the Picower Institute for Learning and Memory in the Department of Brain and Cognitive Sciences at the Massachusetts Institute of Technology.
16 Facts About Li-Huei Tsai
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Li-Huei Tsai is known for her work on neurological disorders that affect learning and memory, particularly for her research on Alzheimer's disease and the role of CDK5 and chromatin remodeling in the progression of the disease.
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In 1991, Li-Huei Tsai joined the laboratory of Ed Harlow at the Cold Spring Harbor Laboratory and then the Massachusetts General Hospital Cancer Center.
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In 1994, Li-Huei Tsai joined the faculty in the Department of Pathology at Harvard Medical School.
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Li-Huei Tsai was appointed director of the Picower Institute for Learning and Memory in 2009 and is a founding member of MIT's Aging Brain Initiative.
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In 2019, Li-Huei Tsai became co-director of the Alana Down Syndrome Center at MIT.
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Li-Huei Tsai became interested in CDK5, which she found was not only inactive in cancer cells, but inactive in all other tissue cells except for the brain.
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Li-Huei Tsai found that Cdk5 requires p35 to be active.
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Li-Huei Tsai found that mice lacking p35 displayed cortical lamination defects and were prone to seizures, and that CDK5-p35 activity was essential for neurite outgrowth during neuronal differentiation.
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Li-Huei Tsai discovered that while Cdk5 activity is essential to proper brain development and function, overexpression of Cdk5 was associated with Alzheimer's disease.
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Li-Huei Tsai observed that a truncated version of p35 called p25 accumulated in diseased or damaged brain tissue in mice and in tissue samples from deceased Alzheimer's patients.
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Li-Huei Tsai was able to replicate the same effects as the enriched environment by treating the mice with a drug that inhibited a chromatin-remodeling class of enzymes called histone deacetylases, or HDACs.
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In later studies, Li-Huei Tsai showed that HDAC2 creates an epigenetic blockade of genes that regulate structural and synaptic plasticity and that some cognitive function could be restored by inhibiting HDAC2 activity.
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Li-Huei Tsai has elucidated the role of structural and epigenetic mechanisms in Alzheimer's disease, showing in two 2015 studies that the DNA breakage necessary to learning was responsible for cognitive decline, due to decline in DNA repair systems with age, and that the genetic component of Alzheimer's primarily affects the regulatory circuitry of immune processes, rather than neuronal processes as expected.
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In 2016, Li-Huei Tsai demonstrated that visual stimulation of mice with an LED flashing at 40 hertz substantially reduces the beta amyloid plaques associated with Alzheimer's disease, likely by inducing gamma oscillations.
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In more recent work, Li-Huei Tsai has created a lab-engineered model of the Blood-Brain Barrier to investigate how Alzheimer disease risk genes, namely APOE, contribute to breakdown of the brain's vasculature.