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Cited by 33

The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.

Cholesterol and Alzheimer's disease

Wolozin, B.·2002·Biochemical Society Transactions
DOI 10.1042/bst0300525
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Abstract

Accumulation of a 40–42-amino acid peptide, termed amyloid-β peptide (Aβ), is associated with Alzheimer's disease (AD), and identifying medicines that inhibit Aβ could help patients with AD. Recent evidence suggests that a class of medicines that lower cholesterol by blocking the enzyme 3-hydroxy-3-methylglutaryl-CoA reductase (HMG-CoA reductase), termed statins, can inhibit Aβ production. Increasing evidence suggests that the enzymes that generate Aβ function best in a high-cholesterol environment, which might explain why reducing cholesterol would inhibit Aβ production. Studies using both neurons and peripheral cells show that reducing cellular cholesterol levels, by stripping off the cholesterol with methyl-β-cyclodextrin or by treating the cells with HMG-CoA reductase inhibitors, decreases Aβ production. Studies performed on animal models and on humans concur with these results. In humans, lovastatin, an HMG-CoA reductase inhibitor, has been shown to reduce Aβ levels in blood of patients by up to 40%. The putative role of Aβ in AD raises the possibility that treating patients with statins might lower Aβ, and thereby either delay the occurrence of AD or retard the progression of AD. Two large retrospective studies support this hypothesis. Both studies suggest that patients taking statins had an approx. 70% lower risk of developing AD. Since statins are widely used by doctors, their ability to reduce Aβ offers a putative therapeutic strategy for treating AD by using medicines that have already been proved safe to use in humans.

Overview

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Crossref · 10.1042/bst0300525

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8 of 8 references verified0 citation errors · 0 not checkable

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  • Cholesterol dysregulation and lipid dyshomeostasis have been identified in several neurodegenerative diseases.

    “Importantly, cholesterol dysregulation6–9 and lipid dyshomeostasis8,10–15 have been identified in several neurodegenerative diseases.”

    From GRAMD1B is a regulator of lipid homeostasis, autophagic flux and phosphorylated tau (2025) · cites this paper as [7]

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Metadata

Authors
Wolozin, B.
Affiliations
Department of Pharmacology, Loyola University Medical Center, Bldg. 102, Rm. 3634, 2160 South First Avenue, Maywood, IL 60153, U.S.A.
Venue
Biochemical Society Transactions
Publisher
Portland Press Ltd.
Published
2002-08-01
Volume
30
Issue
4
Pages
525-529
ISSN
  • 0300-5127
  • 1470-8752
DOI
10.1042/bst0300525
Cited by
33
References
8
Language
en

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