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The tight coupling between neuronal activity and the local increase of bloodflow termed neurovascular coupling is essential for normal brain function. Thismechanism of regulation is compromised in Alzheimer's Disease (AD). In order todetermine whether a purely vascular dysfunction or a neuronal alteration ofblood vessels diameter control could be responsible for the impairedneurovascular coupling observed in AD, blood vessels reactivity in response todifferent pharmacological stimulations was examined in double transgenicAPPxPS1 mice model of AD. Blood vessels movements were monitored using infraredvideomicroscopy ex vivo, in cortical slices of 8 month-old APPxPS1 and wildtype (WT) mice. We quantified vasomotor responses induced either by directblood vessel stimulation with a thromboxane A 2 analogue, the U46619(9,11-dideoxy-11a,9a-epoxymethanoprostaglandin F2) or via the stimulation ofinterneurons with the nicotinic acetylcholine receptor (nAChRs) agonist DMPP(1,1-Dimethyl-4-phenylpiperazinium iodide). Using both types of stimulation, nosignificant differences were detected for the amplitude of blood vesseldiameter changes between the transgenic APPxPS1 mice model of AD and WT mice,although the kinetics of recovery were slower in APPxPS1 mice. We find thatactivation of neocortical interneurons with DMPP induced both vasodilation viaNitric Oxide (NO) release and constriction via Neuropeptide Y (NPY) release.However, we observed a smaller proportion of reactive blood vessels following aneuronal activation in transgenic mice compared with WT mice. Altogether, theseresults suggest that in this mouse model of AD, deficiency in the corticalneurovascular coupling essentially results from a neuronal rather than avascular dysfunction.

Impaired neurovascular coupling in the APPxPS1 mouse model of Alzheimerâs disease

Impaired neurovascular coupling in the APPxPS1 mouse model of Alzheimerâs disease