Minocycline, Microglia, And Amyloidosis

Rong Fan, Feng Xu, Mary Lou Previti, Judianne Davis, Alicia M. Grande, John K. Robinson, and William E. Van Nostrand



Amyloid- (A') can accumulate not only as parenchymal plaques in brain, but also the fibrillary deposits in cerebral vasculature. Early and severe vascular deposits in cerebral amyloid angiopathy (CAA) result from inherited A' mutations and are associated with a strong local neuroinflammatory reaction. The latter seems to correlate with amyloid extending from vessels into brain parenchyma. This week, Fan et al. measured the effects of a neural anti-inflammatory drug in Tg-SwDI mice. Decoding the name, the mouse is a transgenic strain that expresses human amyloid precursor protein carrying the Dutch- and Iowa-type familial CAA mutations. The anti-inflammatory drug minocycline did not affect fibrillar amyloid deposits in the microvasculature of Tg-SwDI mice, nor was total soluble or insoluble A' reduced. Minocycline also did not alter the number of reactive astrocytes. However, minocycline did reduce the number and activation state of microglia. After 4 weeks of treatment, 1-year-old mice displayed improved learning memory performance in a maze task.







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