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Metals in Alzheimer's disease: a systemic perspective.
1Department of Neuroscience, AFaR, Fatebenefratelli Hospital, Rome, Italy. rosanna.squitti@afar.it
Frontiers in Bioscience (Landmark Edition)
|December 29, 2011
Summary
Systemic alterations in copper and iron homeostasis are linked to Alzheimer's disease (AD) pathology. This review suggests viewing local metal accumulation within a broader context of whole-body metal imbalance for AD.
Area of Science:
- Neuroscience
- Biochemistry
- Pathology
Background:
- Alzheimer's disease (AD) involves toxic pathways influenced by metals like copper, iron, and zinc.
- Metals are implicated in the aggregation and neurotoxicity of amyloid-beta (Aβ), a key component of AD plaques.
- Previous research focused on localized metal accumulation in specific brain regions.
Purpose of the Study:
- To review the role of systemic, rather than local, alterations in copper and iron status in Alzheimer's disease.
- To propose a broader framework for understanding metal dyshomeostasis in AD.
Main Methods:
- Review of in vitro, animal, and in vivo studies.
- Analysis of correlations between systemic metal homeostasis and AD markers.
Main Results:
- In vivo studies show that abnormal metal homeostasis correlates with AD deficits.
- Cerebrospinal fluid (CSF) analysis reveals links between metal status and Aβ and Tau proteins.
- Systemic metal alterations provide a wider context for local metal accumulation in AD.
Conclusions:
- Systemic copper and iron dyshomeostasis is a significant factor in Alzheimer's disease.
- Local metal accumulation in the brain should be considered within the scope of systemic metal imbalance.
- Understanding systemic metal alterations may offer new therapeutic avenues for AD.
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