Ann N Y Acad Sci. 2004 Mar;1012:179-182.  Related Articles, Links  

 
Oxidative Stress and Redox-Active Iron in Alzheimer's Disease.

Honda K, Casadesus G, Petersen RB, Perry G, Smith MA.

Institute of Pathology, Case Western Reserve University, Cleveland, Ohio, USA.

Many lines of evidence indicate that oxidative stress is one of the earliest
events in the genesis of Alzheimer's disease (AD). Iron is a transition metal
capable of generating hydroxyl radicals, the most potent reactive oxygen
species. Consequently, a disruption in the metabolism of iron has been
postulated to have a role in the pathogenesis of AD. Indeed, both senile
plaques and neurofibrillary tangles, the major pathological landmarks of AD, as
well as neurons in the earliest stages of the disease, show elevated iron
deposition. However, it is clear that the iron bound to lesion-associated
proteins such as amyloid-beta and tau plays only a minor, late role in the
disease, with the RNA-associated iron found in the neuronal cytoplasm occurring
early and being of paramount importance. In this regard, it is probably not
surprising that there is significant oxidation of cytoplasmic RNA among the
populations of neurons vulnerable to AD. In this review, we consider the role
of iron-induced oxidative stress as a key event in AD pathophysiology.

PMID: 15105265 [PubMed - as supplied by publisher]

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