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Alzheimer's disease (AD)


Mouse studies suggest antagonizing CD36 could help treat cerebral amyloid angiopathy. Symptoms of cerebral amyloid angiopathy include vascular and cognitive dysfunction caused by amyloid deposits in cerebral arteries. In a mouse model of AD expressing mutant amyloid precursor protein (APP), CD36 knockout prevented cerebrovascular dysfunction. CD36 knockout also decreased b-amyloid (Ab) levels in the vasculature and increased both cognitive performance and levels of low-density lipoprotein-related protein 1 a-2-macroglobulin receptor (LRP1; CD91), which clears Ab from the brain, compared with no knockout. Next steps could include developing CD36 antagonists.
Arteria S.A.'s CD36 inhibitor, AP5258, is in preclinical testing to treat dyslipidemia.

SciBX 6(7); doi:10.1038/scibx.2013.167
Published online Feb. 21, 2013

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Park, L. et al. Proc. Natl. Acad. Sci. USA; published online Feb. 4, 2013;
Contact: Costantino Iadecola, Weill Cornell Medical College, New York, N.Y.
Contact: Bruce S. McEwen, The Rockefeller University, New York, N.Y.