Issue Information

Front coverWe have previously demonstrated that a cortical stroke causes persistent impairment of hippocampal-dependent cognitive tasks concomitant with secondary neurodegenerative processes such as amyloid- β accumulation in the hippocampus, a region remote from the primary infarct. There is emerging evidence suggesting that deposition of amyloid-β around cerebral vessels may lead to cerebrovascular structural changes, neurovascular dysfunction, and disruption of blood-brain barrier integrity. Howeve r, there is limited knowledge about the temporal changes of hippocampal cerebrovasculature after cortical stroke. In the current study, we aimed to characterise the spatiotemporal cerebrovascular changes after cortical stroke. We showed, for the first time, sustained cerebrovascular remodelling and vascular leakage (indicative of blood-bran-barrier disruption) in the ipsilateral hippocampus at 84 days post-stroke. Vessel diameter was decreased in the CA1 subregion, which was exacerbated in vessels with amyloid-β deposition. Our findings indicate that hippocampal vasculature may represent an i mportant therapeutic target to mitigate the progression of post-stroke cognitive impairment.Image contentVessels colocalised with amyloid- β (Aβ) have significantly reduced vessel diameters at 84 days post-stroke. Representative immunofluorescence labelling for lectin (cyan), amyloid-β (yellow) and PDGFRβ (magenta). Vessels with amyloid-β deposition showed a decrease in vessel diame...
Source: Journal of Neurochemistry - Category: Neuroscience Tags: ISSUE INFORMATION Source Type: research