Xiaodong Pan

TL;DR: The results imply that Aβ oligomers induce a potent inflammatory response and subsequently disturb microglial phagocytosis and clearance of Aβ fibrils, thereby contributing to an initial neurodegenerative characteristic of AD.

TL;DR: It is suggested that long-term consumption of ginsenoside Rg1 may delay cognitive decline, associated with significant effects on Abeta generation, PKA/CREB activity, as well as BDNF content in the brain.

TL;DR: T4 protects neuronal cells by blocking inflammatory responses of microglial cells to oligomeric Aβ(1‐42) and that T4 acts on the signaling of NF‐κB and JNK, which are involved in the modulation of inflammatory response, suggest T4 may be an effective agent in modulating neuroinflammatory process in AD.

TL;DR: Ginsenoside Rg1 may serve as a promising agent in modulating Aβ-related pathology in Alzheimer's disease by enhancing the binding of nuclear PPARγ to the BACE1 promoter, which may in turn inhibit the transcription and translation of B ACE1, suppress the activity of Bace1, and ultimately attenuate Aβ generation.

TL;DR: OA&bgr;-accelerated neuronal senescence may be associated with the cognitive impairment in 5XFAD mice and can serve as an indicator to estimate the cognitive prognosis for AD population.