Impaired astrocytic Ca signaling in awake-behaving Alzheimer's disease transgenic mice.

Increased astrocytic Ca signaling has been shown in Alzheimer's disease mouse models, but to date no reports have characterized behaviorally induced astrocytic Ca signaling in such mice. Here, we employ an event-based algorithm to assess astrocytic Ca signals in the neocortex of awake-behaving tg-ArcSwe mice and non-transgenic wildtype littermates while monitoring pupil responses and behavior. We demonstrate an attenuated astrocytic Ca response to locomotion and an uncoupling of pupil responses and astrocytic Ca signaling in 15-month-old plaque-bearing mice.

Cerebral Amyloid Angiopathy in a Mouse Model of Alzheimer's Disease Associates with Upregulated Angiopoietin and Downregulated Hypoxia-Inducible Factor.

Background: Vascular pathology is a common feature in patients with advanced Alzheimer's disease, with cerebral amyloid angiopathy (CAA) and microvascular changes commonly observed at autopsies and in genetic mouse models. However, despite a plethora of studies addressing the possible impact of CAA on brain vasculature, results have remained contradictory, showing reduced, unchanged, or even increased capillary densities in human and rodent brains overexpressing amyloid-β in Alzheimer's disease and Down's syndrome.

Objective: We asked if CAA is associated with changes in angiogenetic factors or receptors and if so, whether this would translate into morphological alterations in pericyte coverage and vessel density.