Abstract
This review is focused on discussing in some detail possible neuroprotective functions of microglial cells. We strive to explain how loss of these essential microglial functions might contribute toward the development of characteristic neuropathological features that characterize Alzheimer’s disease. The conceptual framework guiding our thinking is provided by the hypothesis that microglial senescence accounts for impaired neuronal protection and consequent neurodegeneration.
Highlights
The role of CNS microglial cells in the development of Alzheimer’s disease(AD) has been the subject of considerable interest since McGeer’s initial description of reactive microglia in human AD brain in 1987 (McGeer et al, 1987)
We briefly describe our own vision of what may be the role of microglia in AD pathogenesis, which is different in that our primary focus is not on a single protein (Aβ) as the cause of AD, but instead relies on the incontrovertible fact that the incidence of sporadic AD is strongly correlated with aging
The currently popular idea of differentiating functionally distinct macrophage phenotypes classified as M1, M2, and a third,“deactivated” form might apply merely to those few microglial cells that at any given time are in a macrophage state during CNS injury or www.frontiersin.org
Summary
The role of CNS microglial cells in the development of Alzheimer’s disease(AD) has been the subject of considerable interest since McGeer’s initial description of reactive microglia in human AD brain in 1987 (McGeer et al, 1987). In the normal adult brain, microglia display a welldifferentiated, dendritic morphology similar to that of other brain cells They exhibit multiple, finely branched cytoplasmic processes with which they constantly explore the CNS microenvironment searching for disturbances that may require their quick response (Nimmerjahn et al, 2005; Tremblay et al, 2010). These ramified microglia are sensors of pathology (Kreutzberg, 1996; Stence et al, 2001; Petersen and Dailey, 2004; Davalos et al, 2005) and they do not exhibit macrophage morphology, nor do they express the typical macrophage marker, CD68 (recognized by ED1 antibody in the rat). The currently popular idea of differentiating functionally distinct macrophage phenotypes classified as M1 (cytotoxic), M2 (reparative), and a third,“deactivated” form might apply merely to those few microglial cells that at any given time are in a macrophage state during CNS injury or www.frontiersin.org
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