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Link between heart disease, cholesterol, and Alzheimer's disease: A review
Author(s) -
Sparks D. Larry,
Martin Timothy A.,
Gross David R.,
Hunsaker John C.
Publication year - 2000
Publication title -
microscopy research and technique
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 118
eISSN - 1097-0029
pISSN - 1059-910X
DOI - 10.1002/1097-0029(20000815)50:4<287::aid-jemt7>3.0.co;2-l
Subject(s) - cholesterol , disease , alzheimer's disease , amyloid (mycology) , medicine , endocrinology , amyloid beta , reductase , senile plaques , hmg coa reductase , biology , pathology , biochemistry , enzyme
Increased prevalence of Alzheimer's disease‐like β‐amyloid deposits in the neuropil and within neurons occurs in the brains of non‐demented individuals with heart disease. Heart disease is a prevalent finding in Alzheimer's disease, and may be a forerunner to the dementing disorder. In the cholesterol‐fed rabbit model of human coronary heart disease there is production and accumulation of β‐amyloid in the brain. This accumulation of β‐amyloid can be reversed by removing cholesterol from the rabbits' diet. In culture cells, a cholesterol challenge has been shown to increase production of β‐amyloid, and dramatic reductions of cholesterol produced by HMG Co‐A reductase inhibitors decrease production of β‐amyloid. Increased β‐amyloid production is also produced by dietary cholesterol in a number of transgenic mouse models of Alzheimer's disease. Administration of HMG Co‐A reductase inhibitors may block β‐amyloid production caused by dietary cholesterol in rabbits. Clinical trials testing the benefit of HMG Co‐A reductase inhibitors in the treatment of Alzheimer's disease are underway. Microsc. Res. Tech. 50:287–290, 2000. © 2000 Wiley‐Liss, Inc.