Decreased expression of CD36 precedes amyloid accumulation in the 3xTgAD mouse model of Alzheimer’s disease

Alzheimer’s disease (AD) is a disorder characterized by various morphological and functional changes in the brain, prominent among which is the cerebral amyloid β-peptide (Aβ) plaque deposition. Activated glia have been implicated in the clearance of Aβ through the Aβ cell surface class B scavenger receptor CD36. Despite the presence of abundant activated microglia in the brains of AD patients and mouse models of AD, these cells fail to efficiently remove Aβ fibrils. We decided to explore the possibility that decreased expression of CD36 is, in part, responsible for the accumulation of Aβ in AD. To this end, we analyzed the expression of CD36 in young (4 month-old) and older (1 year-old) triple transgenic (3xTgAD) mice that recapitulate the age-dependent AD hallmarks of Aβ deposition and tau hyperphosphorylation. We found that levels of CD36 were significantly lower in the cortex of both young and older 3xTgAD mice compared to age-matched nontransgenic control mice. In contrast, CD36 levels in the cerebellum and spleen (tissues lacking amyloid pathology in 3xTgAD mice) were not different between the 3xTgAD and control mice. The fact that CD36 expression was decreased in the cortex of 3xTgAD mice before evidence of Aβ accumulation, suggests a potential role for CD36 in the process of plaque formation. Studies are currently in progress to directly test such a possibility