Yuyan Cheng

TL;DR: Evidence that inhibition of glycogen synthase kinase-3 (GSK3) ameliorates cognitive deficits in a wide variety of animal models of CNS diseases, including Alzheimer's disease, Fragile X syndrome, Down syndrome, Parkinson's Disease, spinocerebellar ataxia type 1, traumatic brain injury, and others is reviewed.

TL;DR: A new model of prolonged depression-like behavior is described and it is demonstrated that stress-induced GSK3 activation contributes to disruption of BBB integrity mediated by inflammation, particularly TNFα, which contributes to impaired recovery from prolonged learned helplessness.

TL;DR: Stress-induces a broad inflammatory response in mouse hippocampus that involves TLR4, GSK3, and downstream inflammatory signaling, and these stress responses contribute to susceptibility to depression-like behavior in mice.

TL;DR: An emerging target to control detrimental outcomes of stress and inflammation is glycogen synthase kinase-3 (GSK3), which promotes inflammation, partly by regulating key transcription factors in the inflammation signaling pathway, and can impair learning by promoting inflammation and by inhibiting long-term potentiation (LTP).

TL;DR: It is demonstrated that a single stress induces the expression of many cytokines, and that sequential, daily stresses accelerates the rate of cytokine production, which may contribute to deleterious effects of stress on depression and other stress-linked diseases.