Chengbiao Lu

TL;DR: It is found that overexpression of human wild-type full-length tau (termed hTau) induced memory deficits with impairments of synaptic plasticity, and this finding provides a potential drug target for arresting tauopathies.

TL;DR: It is demonstrated that the AD-like tau accumulation induces anxiety through disrupting miR92a-vGAT-GABA signaling, which reveals molecular mechanisms underlying the anxiety behavior in AD patients and potentially leads to the development of new therapeutics for tauopathies.

TL;DR: It is demonstrated that nicotine modulates γ oscillations via α7 and α4β2 nAChR as well as NMDA activation, suggesting that nA ChR activation may have a therapeutic role for the clinical disorder such as schizophrenia, which is known to have impaired γscillation and hypo-NMDA receptor function.

TL;DR: This work finds that overexpression of human wild-type full-length tau induced a significant reduction of α4 subunit of nicotinic acetylcholine receptors (nAChRs) with an increased cleavage of the receptor producing a ~55kDa fragment in primary hippocampal neurons and in the rat brains, while the α4 nAChR currents decreased.