Costantino Iadecola

TL;DR: The first in vivo evidence of blood-brain barrier disruption in the aging hippocampus and in minimal cognitive impairment is provided by Montagne et al.

TL;DR: It is suggested that chronic low-dose AngII may offset the homeostatic control of blood pressure by differentially affecting membrane assembly of NADPH oxidase and ROS production in vasopressin and non-vasopressingin neurons located within the PVN.

TL;DR: It is reported that the increase in blood pressure produced by a 2 week administration of a subpressor dose of Ang II results in an elevation in plasma membrane GluN1 in dendrites of PVN neurons in adult male mice, indicating that NMDA receptor plasticity in PVn neurons significantly contributes to the elevated blood pressure mediated by Ang II.

TL;DR: The FPR results from excitation and the FDR inhibition of reticulospinal sympathoexcitatory axons of RVL; the FPR is a consequence of excitation of axons arising from neurons in an as yet unidentified area of lower brainstem projecting to or through the FN and with collateral branches innervating RVL mono- or polysynaptically.

TL;DR: It emerges that this variant is linked to defects in the blood–brain barrier and subsequent cognitive decline and a link between APOE4 and breakdown of the blood-brain barrier is found.