Microglial Activation in Alzheimers Disease

Johannes   C.M.   Schlachetzki; Michael      Hull

doi:10.2174/156720509790147179

Abstract

Alzheimers disease (AD) is a devastating chronic neurodegenerative disease with currently no available disease modifying treatment. In recent years, the peptide amyloid-β has been proposed as the major pathogenic force in the development and progression of AD. Microglia, the resident immune and phagocytic cells of the brain, are known to constantly scan brain tissue and to respond to various pathological stimuli. Thus, newly formed plaque composed of Aβ seem to activate and recruit microglia in AD transgenic mice. However, the role of microglia is only poorly understood in AD. Microglia may act as a double-edged sword being either detrimental or protective depending on the context. In this mini-review, we discuss the importance of microglia and its receptors in neuroinflammation and plaque clearance. A possible disease modifying role of blood-borne monocytes, which are close relatives of bone-marrow derived microglia, will also be addressed.

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