Redox-Active Iron Is A Sensor Of Cognitive Impairment Associated With
Alzheimer's Disease

An innovative discovery has been reported that highlights the problems
that oxidative stress resulting from iron cumulated in the human brain
can generate in relation with the pathogenesis of Alzheimer's disease
(AD), the brain disorder affecting almost 30 million throughout the
world. The results of research carried out by Drs. Manuel Lavados,
Patricio Fuentes and Leonel Rojo from the laboratory of Professor Dr.
R.B. Maccioni of the School of Medicine of the University of Chile,
and the International Center for Biomedicine, together with his
colleagues, appeared recently in Volume 13, Issue 2 of the prestigious
Journal of Alzheimer's Disease (JAD). For several decades this
laboratory has been acknowledged as one of the main world contributors
to our understanding of AD and the development of tools for its early
diagnosis.

The study focuses on the reactivity of iron in the cerebrospinal fluid
(CSF) and its correlation with the severity of cognitive decline in
both patients with AD and subjects diagnosed with mild cognitive
impairment (MCI). Different stages of cognitive and functional
impairment are associated with changes in CSF reactive iron. CSF
samples from 56 seniors classified into 4 groups according to their
scores on the Clinical Dementia Rating scale (CDR) were compared in
respect to the levels of a particular form of iron, the redox-active
iron.

Interestingly, redox-active iron levels in the CSF increased with the
degree of cognitive impairment from normal to MCI subjects, while AD
patients showed an abrupt decrease to levels close to zero. However,
no difference in the total CSF iron was found between the different
groups. Given the relevance of oxidative damage in neurodegeneration
occuring during the course of dementia, the development of cognitive
and functional decline appears to be associated with the presence of
redox-active iron in the CSF. The abrupt decrease in redox-active iron
found in patients affected 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¦Â) 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-¦Â protein precursor (A¦ÂPP) in the
neuronal membrane, while the soluble form of A¦ÂPP (A¦Â peptide) could
act as an iron chelator promoting A¦Â 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.

----------------------------
Article adapted by Medical News Today from original press release.
----------------------------

"Mild Cognitive Impairment and Alzheimer Patients Display Different
Levels of Redox-Active CSF Iron" by Manuel Lavados, Marta Guillen,
Maria Cristina Mujica, Leonel E. Rojo, Patricio Fuentes, Ricardo B.
Maccioni, JAD 13:2, pp 225-232.

Source: Astrid Engelen
IOS Press

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