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Curr Transl Geriatr Exp Gerontol Rep. 2012 Mar;1(1):11-20. Epub 2012 Jan 19.

Animal Models of Alzheimer's Disease: Utilization of Transgenic Alzheimer's Disease Models in Studies of Amyloid Beta Clearance.

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1
A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, P.O. Box 1627, 70211 Kuopio, Finland.

Abstract

Glial cells in Alzheimer's disease (AD) have been shown to be capable of clearing or at least restricting the accumulation of toxic amyloid beta (Aβ) deposits. Recently, bone marrow (BM)-derived monocytic cells have been recognized in experimental studies to be superior in their phagocytic properties when compared to their brain endogenous counterparts. In human AD, BM-derived monocytic cells may have deficiencies in their capacity to restrict plaque growth. Therefore, enhancement of phagocytic properties of cells of monocyte origin, both brain endogenous microglia and BM-derived monocytic cells, offers an attractive therapeutic approach to fight off AD. Transgenic mouse models with aberrant Aβ deposition offer a valuable tool for discovery of novel pathways to facilitate cell-mediated Aβ uptake. This article reviews the most recent findings on the phagocytic capacity of cells with monocytic origin in various transgenic AD models and describes the methods to study phagocytic activity of these cells.

KEYWORDS:

Aging; Alzheimer’s disease; Amyloid beta; Amyloid precursor protein; Bone marrow; Chemokines; Cognitive function; Cytokines; Inflammation; Lysosomes; Macrophages; Microglia; Phagocytosis; Presenilins; Transgenic mice

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