Abnormal localization of iron regulatory protein in Alzheimer's disease

A role for altered iron metabolism in the pathogenesis of Alzheimer's disease has been suggested by several reports associating the cardinal neuropathologic lesions with markers of free radical-induced damage and redox-active iron. We hypothesized that the abnormal distribution of iron in Alzhe...

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Bibliographic Details
Published in:Brain research 1998-03, Vol.788 (1), p.232-236
Main Authors: Smith, Mark A., Wehr, Kristina, Harris, Peggy L.R., Siedlak, Sandra L., Connor, James R., Perry, George
Format: Article
Language:English
Subjects:
Aged
Aged, 80 and over
Alzheimer Disease - metabolism
Alzheimer's disease
Biological and medical sciences
Case-Control Studies
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
Energy Metabolism - physiology
Homeostasis
Humans
Immunohistochemistry
Iron
Iron Regulatory Protein 1
Iron Regulatory Protein 2
Iron-Regulatory Proteins
Iron-Sulfur Proteins - analysis
Medical sciences
Metabolism
Middle Aged
Nerve Tissue Proteins - analysis
Neurology
Oxidation-Reduction
Oxidative stress
Oxidative Stress - physiology
RNA-Binding Proteins - analysis
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Summary:A role for altered iron metabolism in the pathogenesis of Alzheimer's disease has been suggested by several reports associating the cardinal neuropathologic lesions with markers of free radical-induced damage and redox-active iron. We hypothesized that the abnormal distribution of iron in Alzheimer brain might result from alterations in iron regulatory proteins (IRP) such as IRP-1 and IRP-2, the main control elements of cellular iron homeostasis. Here, we report that while IRP-1 is present at similar levels in both Alzheimer and control brain tissue, IRP-2 shows striking differences and is associated with intraneuronal lesions, including neurofibrillary tangles, senile plaque neurites and neuropil threads. Since IRP-2 colocalizes with redox-active iron, our results suggest that alterations in IRP-2 might be directly linked to impaired iron homeostasis in Alzheimer's disease.
ISSN:0006-8993
1872-6240
DOI:10.1016/S0006-8993(98)00002-X