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Redox-active iron is a sensor of cognitive impairment associated with Alzheimer's disease
Date:4/4/2008

d with AD may represent a terminal situation, whereby the central nervous system attempts to minimize iron-associated toxicity.

A possible mechanism to explain the decrease of redox-active CSF iron during the course of the disease could be the sequestration of this metal by the aggregation of a brain component called amyloid peptides (A) into the senile plaques, anomalous structures where cumulative iron has been found. High redox-active CSF iron levels could increase the production of the amyloid- protein precursor (APP) in the neuronal membrane, while the soluble form of APP (A peptide) could act as an iron chelator promoting A peptides aggregation into the senile plaques. The suggested mechanism could represent a homeostatic process by the brain that fights to reduce the cascade of cellular insults in AD, in order to regulate the CSF iron levels and its toxicity. These findings indicate that the decrease in redox-active CSF iron may correspond to a final late effort by brain cells to decrease oxidative stress mediated by iron.

This discovery offers the possibility to monitor iron levels in the CSF in relation with cognitive impairment and perhaps be used as part of a battery of biomarkers for an early diagnosis of these disorders, thus facilitating the appropriate treatment to patients and increasing their quality of life.


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Contact: Astrid Engelen
a.engelen@iospress.nl
31-206-883-355
IOS Press
Source:Eurekalert

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