. Local self-renewal can sustain CNS microglia maintenance and function throughout adult life. Nat Neurosci. 2007 Dec;10(12):1538-43. PubMed.

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  1. The protean and itinerant nature of phagocytes has compelled researchers to devise increasingly ingenious experiments to establish their role in brain disorders, as exemplified nicely by the studies of Mildner et al. and Ajami et al. These researchers make a reasonably compelling case that significant infiltration of the brain by peripheral, bone marrow-derived macrophages requires a weakening of normal host barriers. Since phagocytes exist on both sides of the cerebrovascular wall, does it matter to the brain where the cells come from? I think it does; there is growing evidence for functional specialization in otherwise similar-appearing macrophages, and (from an evolutionary perspective) why would the brain be endowed with such an effective—and selective—obstacle to circulating phagocytes if their pedigree was unimportant?

    Regarding the enduring discussion of the role of phagocytes in Alzheimer disease, one additional issue—cerebral β amyloid angiopathy (CAA)—is worth a comment. The degree of CAA in Alzheimer disease is highly variable, but affected vessels can be appreciably impaired, as evidenced by an elevated risk of hemorrhagic stroke. It is therefore conceivable that CAA might augment the infiltration of circulating monocytes into the brain, thereby modifying the pathologic signature and course of disease. On the flip side, the presence of CAA could reflect subtle functional differences in brain phagocytes. El Khoury et al., 2007 found that the disruption of microglial accumulation via Ccr2 deficiency causes the early appearance of CAA and microhemorrhage in APP-transgenic mice. Phagocytes thus may help to regulate the compartmentalization of Aβ aggregates in brain, suggesting that the presence and phenotype of these cells can influence the risk of CAA in older humans.

    References:

    . Ccr2 deficiency impairs microglial accumulation and accelerates progression of Alzheimer-like disease. Nat Med. 2007 Apr;13(4):432-8. PubMed.

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