CCR2 SHOWS A MICROGLIA NEUROPROTECTIVE
ROLE
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.