Literature DB >> 24189189

Prolonged exposure to low levels of aluminum leads to changes associated with brain aging and neurodegeneration.

Stephen C Bondy1.   

Abstract

Aluminum is one of the most common metal elements in the earth's crust. It is not an essential element for life and has commonly been thought of as a rather inert and insoluble mineral. Therefore, it has often been regarded as not posing a significant health hazard. In consequence, aluminum-containing agents been used in many food processing steps and also in removal by flocculation of particulate organic matter from water. In recent years, acid rain has tended to mobilize aluminum-containing minerals into a more soluble form, ionic Al(3+), which has found their way into many reservoirs that constitute residential drinking water resources. As a result, the human body burden of aluminum has increased. Epidemiological studies suggest that aluminum may not be as innocuous as was previously thought and that aluminum may actively promote the onset and progression of Alzheimer's disease. Epidemiological data is strengthened by experimental evidence of aluminum exposure leading to excess inflammatory activity within the brain. Such apparently irrelevant immune activity unprovoked by an exogenous infectious agent characterizes the aging brain and is even more pronounced in several neurodegenerative diseases. The causation of most of these age-related neurological disorders is not understood but since they are generally not genetic, one must assume that their development is underlain by unknown environmental factors. There is an increasing and coherent body of evidence that implicates aluminum as being one such significant factor. Evidence is outlined supporting the concept of aluminum's involvement in hastening brain aging. This acceleration would then inevitably lead to increased incidence of specific age-related neurological diseases.
Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.

Entities:  

Keywords:  Aluminum toxicity; Brain senescence; Neuroinflammation; Neurological disease; Oxidative stress

Mesh:

Substances:

Year:  2013        PMID: 24189189     DOI: 10.1016/j.tox.2013.10.008

Source DB:  PubMed          Journal:  Toxicology        ISSN: 0300-483X            Impact factor:   4.221


  28 in total

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9.  Spermine protects aluminium chloride and iron-induced neurotoxicity in rat model of Alzheimer's disease via attenuation of tau phosphorylation, Amyloid-β (1-42) and NF-κB pathway.

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10.  Toxicant exposure and bioaccumulation: a common and potentially reversible cause of cognitive dysfunction and dementia.

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