Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2009 Dec;6(6):554-63.
doi: 10.2174/156720509790147179.

Microglial activation in Alzheimer's disease

Johannes C M Schlachetzki  1 , Michael Hüll
Affiliations
Review

Microglial activation in Alzheimer's disease

Johannes C M Schlachetzki et al. Curr Alzheimer Res. 2009 Dec.

Abstract

Alzheimer's disease (AD) is a devastating chronic neurodegenerative disease with currently no available disease modifying treatment. In recent years, the peptide amyloid-beta 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 A beta 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.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

Publication types

Substances