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Review
. 2006 Jul;155(1):45-51.
doi: 10.1016/j.jsb.2005.12.011. Epub 2006 Feb 9.

Metal exposure and Alzheimer's pathogenesis

Guijian Liu  1 , Weidong Huang, Robert D Moir, Charles R Vanderburg, Barry Lai, Zicheng Peng, Rudolph E Tanzi, Jack T Rogers, Xudong Huang
Affiliations
Review

Metal exposure and Alzheimer's pathogenesis

Guijian Liu et al. J Struct Biol. 2006 Jul.

Abstract

With the growing aging population in Western countries, Alzheimer's disease (AD) has become a major public health concern. No preventive measure and effective treatment for this burdensome disease is currently available. Genetic, biochemical, and neuropathological data strongly suggest that Abeta amyloidosis, which originates from the amyloidogenic processing of a metalloprotein-amyloid precursor protein (APP), is the key event in AD pathology. However, neurochemical factors that impact upon the age-dependent cerebral Abeta amyloidogenesis are not well recognized. Growing data indicate that cerebral dysregulation of biometals, environmental metal exposure, and oxidative stress contribute to AD pathology. Herein we provided further evidence that both metals (such as Cu) and H(2)O(2) promote formation of neurotoxic Abeta oligomers. Moreover, we first demonstrated that laser capture microdissection coupled with X-ray fluorescence microscopy can be applied to determine elemental profiles (S, Fe, Cu, and Zn) in Abeta amyloid plaques. Clearly the fundamental biochemical mechanisms linking brain biometal metabolism, environmental metal exposure, and AD pathophysiology warrant further investigation. Nevertheless, the study of APP and Abeta metallobiology may identify potential targets for therapeutic intervention and/or provide diagnostic methods for AD.

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