Figure 3.

Aβ accumulation and aggravation under CCH. (I,II) The abundant BDNF produced by endothelium in the NVU can bind to TrkB receptors on OPCs and neurons to promote their proliferation, migration and survival, which can be disrupted by CCH. (III) CCH can significantly decrease A1R expression and subsequently impede neuron hyperpolarizes in the post-synapse through G-protein coupled inwardly rectifying K⁺ channels. (IV) AQP4, as a water channel, is generally restricted to astrocytic end-feet processes that mainly contact synapses and vasculature. Additionally, AQP4 also plays an important role in maintaining osmotic balance through eliminating edema induced by various damages. CCH can lead to AQP4 mislocalization and then induce extensive trophic uncoupling and osmotic imbalance, ultimately destroying CBF regulation and attenuating perfusion to the brain.