Research Interest:

Alzheimer's disease (AD) is a devastating neurodegenerative disorder affilicting more than 35 million people worldwidely. It was estimated that the prevalence of AD will be tripled in 2050 if no cure is found. Amount of evidence suggests that accumulation of amyloid β (Aβ), the proteolytic product of amyloid precursor protein (APP), is one of the key causal factors for AD, and tau is necessary for Aβ to induce synaptic, neuronal, and circuitry deficits in AD. However, the exact mechnisms underlying Aβ-induced neuronal toxicity and abnormal circuitry/network activity remain elusive. As shown below, my group is intersted in the possible involvement of GABAergic interneurons and adult newborn neurons in Aβ-induced deficits found in AD. We hypothesize that GABAergic interneurons are essential for neural network activiy and adult hippocampal neurogenesis, abnormal accumulation of Aβ in the brain would damage GABAergic interneurons and therefore result in neural network dysfunction and impairment of adult neurogenesis, which will lead to cognitive deficits in AD. Modulating GABAergic interneurons or newborn neurons may counteract Aβ-induced toxicity. 

Grant Supports:

1. Network modulation between niche and adult neural stem cells. National Program on Key Basic   Research Project from the Ministry of Science and Technology of China (2014CB964602), 2014-2018

2. Effects of modulating PV interneurons on Aβ-induced neuropathology. Distinguished Young Scholar Program, Zhejiang Provincial Natural Science Foundation (LR13H090001), 2013-2016

3. Roles of adult hippocampal newborn neurons in Aβ-induced neural circuitry deficits. Major Research Plan, National Natural Science Foundation of China (91132713), 2012-2014