Copyright 2009 Elsevier Ltd. All rights reserved.

Encyclopedia of Neuroscience
Binder, Marc D.; Hirokawa, Nobutaka; Windhorst, Uwe (Eds.) Version: eReference (online access) 2009 ISBN: 978-3-540-29678-2

Aluminum
S.C. Bondya
a

University of California at Irvine, Irvine, CA, USA

Available online 4 November 2008.

Abstract
Evidence for the potential hazard of chronic exposure to low levels of aluminum is derived from both epidemiological and biochemical studies. The promotion of excess levels of neuroinflammation and oxidative stress may form the basis of damage to the central nervous system. These factors can potentially cause aluminum to accelerate brain aging and, more specifically, to enhance the progression of Alzheimer's disease. In this article, the basic chemistry and distribution of aluminum in the environment are described. The sources and occurrence of the acute neurotoxic effects of systemic aluminum are also outlined and potential mechanisms underlying the toxicity of apparently inert aluminumcontaining minerals are discussed.

Author Keywords: Aluminum ; Alzheimer's disease; Astroglia; Brain aging; Cytokines; Inflammation; Microglia; Neurotoxicity; Oxidative stress; Transition metals

Article Outline
Introduction Background and Chemistry Aluminum Prevalence in the Human Environment Aluminum Entry into Nervous Tissues Aluminum and Neurological Disease Dialysis Encephalopathy Evidence of Aluminum Neurotoxicity following Occupational Exposures Other Studies Suggesting that Aluminum Salts Can Be Neurotoxic, and the Safety of Alum-Containing Vaccines Alzheimer's Disease Mechanisms of Neurotoxicity Oxidative Stress Inflammation Conclusions Further Reading

Figure 1. Microglial activation in the brain of aluminum lactate-exposed animals. (a) Control, (b) Al lactate (0.01 mM), (c) Al (0.1 mM); FC, frontal cortex; CC, corpus callosum; CN/P, caudate nucleus/putamen; GP, globus pallidus. 20 magnification.

Figure 2. Proposed trajectory of aluminum (Al)-induced promotion of inflammatory processes within the central nervous system. GI, gastrointestinal; TLR, Toll-like receptor; TNFR1, tumor necrosis factor receptor 1; TNF-, tumor necrosis factor-; NF-B, nuclear factor-kappa B; IL-6, interleukin-6; ROS, reactive oxygen species.

Cross References
Alzheimer's Disease: An Overview Alzheimer's Disease: Molecular Genetics Brain Composition: Age-Related Changes Inflammation in Neurodegenerative Disease and Injury Lipids and Membranes in Brain Aging Metal Accumulation during Aging Neurotoxins and their Neurotoxicology Oxidative Damage in Neurodegeneration and Injury