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Am J Neurodegener Dis 2012;1(3):199-204
Microglial chemotactic signaling factors in Alzheimer’s disease
James G McLarnon
Department of Anesthesiology, Pharmacology and Therapeutics, Faculty of Medicine, The University of British
Columbia, 2176 Health Sciences Mall, Vancouver, BC, Canada V6T 1Z3
Received September 5, 2012; Accepted October 30, 2012; Epub November 18, 2012; Published November 30, 2012
Abstract: The net migration of microglia induced by deposits of amyloid beta (Aβ) constitutes a chemotactic response
of resident neuroimmune brain cells. This process serves to localize clusters of microglia nearby Aβ deposits
preparatory to cellular activation and functional responses. Microglial responses to Aβ deposits localized in brain
parenchyma and in blood vessels lead to acute and chronic neuroinflammation in Alzheimer’s disease (AD) brain.
This review summarizes studies on the prominent chemotactic factors MCP-1, MIP-1α and IL-8 and also includes
recent work indicating VEGF and fractalkine as chemotactic agents. The possibility that microglial release of MCP-1
may play a role in mediating chemotactic responses of neural progenitor cells is also considered. The plethora of
chemotactic factors and their cognate receptors suggests the utility in testing pharmacological modulation of
chemotaxis for effects to inhibit chronic neuroinflammation and confer neuroprotection in AD animal models.
Keywords: Chemotactic factors, microglial chemotaxis, Alzheimer’s disease (AD), inflammatory responses, AD animal
Address all correspondence to:
Dr. James G McLarnon
Anesthesiology, Pharmacology and Therapeutics
2176 Health Sciences Mall, University of British Columbia
Vancouver, BC V6T1Z3, Canada.
Tel: (604) 822-5719; Fax: (604)822-6012