What We Know, What We Don't Know

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Home: Research: Forums: Live Discussions

What We Know, What We Don't Know

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	What we know	What we don’t know
38.	Brain inflammation/gliosis is characteristic of AD	When, how specific, how important?

	Comments

	Comment by: Joseph El Khoury
	Submitted 20 March 2007 \| Permalink	Posted 21 March 2007
	I would add that recent evidence from animal models of AD suggests the following: 1. At least part of the inflammatory response in AD is due to recruitment of blood/bone marrow-derived mononuclear phagocytes (monocytes and/or microglial precursors). 2. The early inflammatory response appears to be beneficial, in that it mediates the clearance of Aβ. 3. It is not clear at what stage of AD pathology the inflammatory response becomes detrimental, further contributing to neurotoxicity. Does the switch occur before formation of visible plaques? Is it due to soluble/oligomeric Aβ, or to fibrillar Aβ? References: Simard AR, Soulet D, Gowing G, Julien JP, Rivest S. Bone marrow-derived microglia play a critical role in restricting senile plaque formation in Alzheimer's disease. Neuron. 2006 Feb 16;49(4):489-502. Abstract Khoury JE, Toft M, Hickman SE, Means TK, Terada K, Geula C, Luster AD. Ccr2 deficiency impairs microglial accumulation and accelerates progression of Alzheimer-like disease. Nat Med. 2007 Mar 11; [Epub ahead of print] Abstract View all comments by Joseph El Khoury

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