Metals In Alzheimer's Disease

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Alzheimer's disease (AD) is a devastating condition and its causes are still largely unknown. Various metals have been implicated as possible contributors to the development of AD. In a special double issue of the Journal of Alzheimer's Disease published in November 2006, guest editors Andrei C. Miu and Oana Benga have brought together 14 insightful articles that explore the roles that metals play in the biochemistry and physiology of AD. The articles cover six major categories: Comprehensive historical reviews, methodological perspectives, a topical review, integrative genetic and epigenetic reports, a review of risk factors and a "benchmark to clinical" review:
- the four-decades-old controversy about aluminum neurotoxicity, examining data on the possible cellular mechanisms underlying aluminum neurotoxicity and potential neuroprotective strategies against aluminum toxicity.
- how metal ions such as zinc and copper can potentiate Alzheimer's disease by participating in the aggregation of normal cellular proteins and in the generation of reactive oxygen species.
- how aluminum and copper can initiate or propagate an inflammatory response in the aging brain.
- metals found in plaque cores in AD brains and concludes that aluminum and iron could cause oxidative damage but copper and zinc likely do not.
- history of aluminum's hypothetical role in AD and several lines of evidence for involvement of aluminum as a secondary aggravating factor or risk factor and argue that further studies are warranted.
- the methodologies that have been used to identify Alzheimer- and dementia-related targets for exogenous toxins.
- recent approaches to locate and identify iron compounds in neurodegenerative tissue. In addition to complementary techniques that allow them to quantify and identify iron compounds using magnetometry, extraction and electron microscopy, they utilize a powerful combined mapping/characterization approach with synchrotron X-rays.
- the movement of metals across the blood-brain barrier and a number of transporters are described that could mediate metal transport into and out of the brain.
- model of amyloid-beta induced heme-deficiency that could account for neurodegeneration in AD patients.
- how presenelins can trigger a cascade of processes that lead to amyloid-beta production, leading to AD.
- the apoE4 isoform of apolipoprotein E and the nucleation, growth and reversibility of amyloid-beta deposition in mice should shed new light on this genetic risk factor for AD.
- the possible role of macronutrients and the basic elements of carbohydrates, proteins, and fat in the development of AD.
- the role of aluminum and metals such as copper and zinc in AD, as well as on metal chelator therapy as a potential treatment for AD. The effects of aluminum, copper and zinc chelating agents on amyloid-beta plaques are reviewed.

Healthy diets, antioxidant supplements, and the prevention of nutritional deficiencies or exposure to foods and water with high content of metals could be considered the first line of defense against the development and progression of cognitive decline.