Microglia, the immune cells of the brain, accumulate in plaques in the brains of patients with Alzheimer’s disease (AD), but whether their presence is beneficial or harmful has long been debated. Last year Simard et al. described a massive infiltration of highly ramified and elongated microglia within the core of amyloid plaques in a transgenic mouse model of the disease, and they demonstrated that most of these cells originate from the bone marrow (Views and News 02-25-06 Blood derived microglia can reduce plaques in Alzheimer’s disease).

It seems that these blood-derived microglia and not their resident counterparts have the ability to eliminate amyloid deposits. However, many researchers still doubt the beneficial role of these newly recruited cells.

CC-chemokine receptor 2 (CCR2) is expressed by microglia and may facilitate their recruitment to the brain, El Khoury and his colleagues showed that knocking out Ccr2 in a transgenic mouse model of AD, reduced microglia accumulation, increased the accumulation of amyloid-β protein and accelerated disease progression in these animals (El Khoury et al. Ccr2 deficiency impairs microglial accumulation and accelerates progression of Alzheimer-like disease. Nature Medicine 13, 432-438, 2007).

This provides support for a neuroprotective role of microglia, which are likely to be involved in amyloid-β clearance.


BM&L-June 2007