Tsai found that mice lacking p35 displayed cortical lamination defects and were prone to seizures,[9] and that CDK5-p35 activity was essential for neurite outgrowth during neuronal differentiation.
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.
[14][15] In later studies, Tsai showed that HDAC2 creates an epigenetic blockade of genes that regulate structural and synaptic plasticity[16] and that some cognitive function could be restored by inhibiting HDAC2 activity.
[21][22] In 2016, 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.
[23][24] In more recent work, 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.