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- W3025493721 abstract "Ameliorating blood–brain barrier disruption and altering scar formation dynamics are potential strategies that may improve post-stroke recovery. CD36 is a class B scavenger receptor that plays a role in innate immunity, inflammation and vascular dysfunction and regulates post-stroke injury, neovascularization, reactive astrogliosis and scar formation. By subjecting WT and CD36KO mice to different MCAo occlusion durations to generate comparable acute lesion sizes, we addressed the role of CD36 in BBB dysfunction, scar formation and recovery. The majority of stroke recovery studies primarily focus on motor function. Here, we employed an extensive behavioral test arsenal to evaluate psychological and cognitive endpoints. While not evident during the acute phase, CD36 deficient mice displayed significantly attenuated BBB leakage and scar formation at three months after stroke compared to wild-type littermates. Assessment of motor (open field, rotarod), anxiety (plus maze, light-dark box), depression (forced swim, sucrose preference) and memory tests (water maze) revealed that CD36 deficiency ameliorated stroke-induced behavioral impairments in activity, hedonic responses and spatial learning and strategy switching. Our findings indicate that CD36 contributes to stroke-induced BBB dysfunction and scar formation in an injury-independent manner, as well as to the chronic motor and neurophysiological deficits in chronic stroke." @default.
- W3025493721 created "2020-05-21" @default.
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- W3025493721 creator A5074827984 @default.
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- W3025493721 date "2020-05-13" @default.
- W3025493721 modified "2023-10-16" @default.
- W3025493721 title "CD36 deficiency reduces chronic BBB dysfunction and scar formation and improves activity, hedonic and memory deficits in ischemic stroke" @default.
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- W3025493721 doi "https://doi.org/10.1177/0271678x20924099" @default.
- W3025493721 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7922745" @default.
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- W3025493721 hasPublicationYear "2020" @default.
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