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P.H. Frederikse, L. Partyka, P. Pierce; Increased Alzheimer Beta–Amyloid Peptides in Lenses in Animals on a High Cholesterol Diet . Invest. Ophthalmol. Vis. Sci. 2006;47(13):2531.
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© ARVO (1962-2015); The Authors (2016-present)
Our lab has been investigating the striking degree of shared cell biology, developmental mechanisms, and gene expression in lens and brain, to understand shared mechanisms of age–related degenerative disease fundamental to both tissues. Work from this, and now from other, laboratories highlight a fundamental role for Alzheimer proteins in lens age–related disease. Moreover, this fundamental link can be exploited for diagnosis of the onset and severity of AD in brain. Considerable evidence in AD research demonstrates that system–wide factors in the body, and most strikingly high cholesterol in the diet together with copper bioavailabilty, have a key role in determining onset and severity of AD brain pathology in humans and in animal models. Further these factors are also critical determinants of cataract formation in the lens. Here we examined the role of Alzheimer proteins in animals on high cholesterol diet with 0.12 ppm Cu in water (10–fold under EPA standards for humans).
Rabbits placed on a high cholesterol diet with or without added copper in drinking water were examined for Alzheimer beta amyloid peptides in lens and brain. Abeta was quantified using ELISA assays and comparative histological examination.
Aß 1–40 and Aß 1–42 peptides increase in animal lenses on a high cholesterol diet with added copper in drinking water, parallelling results in brain on this dietary regimen (Sparks and Schreurs PNAS 2003; 100:: 11065).
The present data demonstrate a coincident production of Alzheimer–linked pathology involving Aß peptide accumulation in lens and brain in animals placed on a well–characterized systemic model of AD on high cholesterol and added dietary copper.
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