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Cognitive Deterioration and Associated Pathology Induced by Chronic Low-Level Aluminum Ingestion in a Translational Rat Model Provides an Explanation of Alzheimer's Disease, Tests for Susceptibility and Avenues for Treatment

Authors :
J. R. Walton
Source :
International Journal of Alzheimer's Disease, Vol 2012 (2012)
Publication Year :
2012
Publisher :
Hindawi Limited, 2012.

Abstract

A translational aging rat model for chronic aluminum (Al) neurotoxicity mimics human Al exposure by ingesting Al, throughout middle age and old age, in equivalent amounts to those ingested by Americans from their food, water, and Al additives. Most rats that consumed Al in an amount equivalent to the high end of the human total dietary Al range developed severe cognitive deterioration in old age. High-stage Al accumulation occurred in the entorhinal cortical cells of origin for the perforant pathway and hippocampal CA1 cells, resulting in microtubule depletion and dendritic dieback. Analogous pathological change in humans leads to destruction of the perforant pathway and Alzheimer's disease dementia. The hippocampus is thereby isolated from neocortical input and output normally mediated by the entorhinal cortex. Additional evidence is presented that Al is involved in the formation of neurofibrillary tangles, amyloid plaques, granulovacuolar degeneration, and other pathological changes of Alzheimer’s disease (AD). The shared characteristics indicate that AD is a human form of chronic Al neurotoxicity. This translational animal model provides fresh strategies for the prevention, diagnosis, and treatment of AD.

Details

Language :
English
ISSN :
20908024 and 20900252
Volume :
2012
Database :
Directory of Open Access Journals
Journal :
International Journal of Alzheimer's Disease
Publication Type :
Academic Journal
Accession number :
edsdoj.289b60a0ea4e9e8b2a1aee3293f332
Document Type :
article
Full Text :
https://doi.org/10.1155/2012/914947