Yizhi Song

TL;DR: In this paper, a review of NMDAR-dependent synaptic depression and spine elimination in Alzheimer's disease is presented, focusing on not only changes in expression of different subunits, but also some unconventional modes of action.

TL;DR: Protective effects of CDNF on Aβ-induced synaptotoxicity and ER stress are revealed, implying that CDNF may protect against A β-inducedSynaptic dysfunction through suppression of ER stress, and could be a potential drug candidate for early AD treatment.

TL;DR: It is demonstrated that long-term sustainable activation of astroglial NF-kappaB following systemic inflammation was associated with brain cell and microvasculature injury in the sub-region of the hippocampus which ultimately likely results in brain functional impairment.

TL;DR: It is demonstrated that astrocytes express NMDARs and therefore have the potential to modulate the synaptotoxic actions of Aβ and therefore be suitable druggable targets for the prevention and/or delay of the synaptic loss that occurs during early stages of AD.

TL;DR: Results show that Aβ exerts complex and distinct regulatory effects on the trafficking and phosphorylation of GluN2A and Glu N2B, as well as on their localization within synaptic and non-synaptic sites.