Affiliations: [a] Departments of Cell and Molecular Biology, John A. Burns School of Medicine, University of Hawai'i, Honolulu, HI, USA | [b] Departments of Gerontology, John A. Burns School of Medicine, University of Hawai'i, Honolulu, HI, USA | [c] Kuakini Medical Center and the Pacific Health Research Institute, Honolulu, HI, USA
Correspondence:
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Corresponding author: Frederick P. Bellinger, Assistant Researcher, Cell and Molecular Biology Department, University of Hawai'i, 651 Ilalo Street, Honolulu, HI 96813, USA. Tel.: +1 808 692 1512; Fax: +1 808 692 1970; E-mail: fb@hawaii.edu.
Abstract: Selenium is known for its antioxidant properties, making selenoproteins candidate molecules for mitigation of neurological disorders in which oxidative stress has been implicated. The selenium transport protein, selenoprotein P, is essential for neuronal survival and function. We sought to determine whether selenoprotein P expression is associated with Alzheimer's disease pathology. We examined postmortem tissue from individuals with the hallmark lesions of Alzheimer's disease and individuals without these lesions. Selenoprotein P immunoreactivity was co-localized with amyloid-β plaques and neurofibrillary tangles. Dense-core and other non-diffuse amyloid-β plaques were nearly always associated with selenoprotein P immunopositive cells. Analysis of spatial distribution showed a significant association between amyloid-β plaques and selenoprotein P. Numerous cells also exhibited immunoreactivity to selenoprotein P and intraneuronal neurofibrillary tangles. Confocal microscopy confirmed co-localization of amyloid-β protein and selenoprotein P. These findings suggest an association of selenoprotein P with Alzheimer's pathology.
Keywords: Alzheimer's disease, amyloid-β, antioxidant, human cortex, neurofibrillary tangle, oxidative stress, selenoprotein, selenoprotein P
