2004Current Opinion in LipidologyRequires access

Cholesterol, statins and dementia

Benjamin Wolozin

Open publisher page 90 citations

Abstract

PURPOSE OF REVIEW: Advances in cholesterol biology suggest that cholesterol metabolism modulates beta-amyloid production, and that pharmaceuticals that inhibit cholesterol metabolism might be valuable in therapy of Alzheimer's disease. Although the genetics and cell biology continue to support the link between cholesterol and Alzheimer's disease, recent clinical studies suggest that the animal studies might not directly translate to clinical studies in humans. RECENT FINDINGS: This review will highlight advances in genetics, cell biology and clinical sciences investigating the relationship between cholesterol and Alzheimer's disease. SUMMARY: Cholesterol, its catabolites and proteins that regulate cholesterol levels all modulate processing of amyloid precursor protein. Statins hold promise in therapy of Alzheimer's disease, but the current data are more consistent with a model of statins that act as neuroprotective agents rather than inhibitors of beta-amyloid production.

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PURPOSE OF REVIEW: Advances in cholesterol biology suggest that cholesterol metabolism modulates beta-amyloid production, and that pharmaceuticals that inhibit cholesterol metabolism might be valuable in therapy of Alzheimer's disease. Although the genetics and cell biology continue to support the link between cholesterol and Alzheimer's disease, recent clinical studies suggest that the animal studies might not directly translate to clinical studies in humans. RECENT FINDINGS: This review will highlight advances in genetics, cell biology and clinical sciences investigating the relationship between cholesterol and Alzheimer's disease. SUMMARY: Cholesterol, its catabolites and proteins that regulate cholesterol levels all modulate processing of amyloid precursor protein. Statins hold promise in therapy of Alzheimer's disease, but the current data are more consistent with a model of statins that act as neuroprotective agents rather than inhibitors of beta-amyloid production.

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Available abstract

PURPOSE OF REVIEW: Advances in cholesterol biology suggest that cholesterol metabolism modulates beta-amyloid production, and that pharmaceuticals that inhibit cholesterol metabolism might be valuable in therapy of Alzheimer's disease. Although the genetics and cell biology continue to support the link between cholesterol and Alzheimer's disease, recent clinical studies suggest that the animal studies might not directly translate to clinical studies in humans. RECENT FINDINGS: This review will highlight advances in genetics, cell biology and clinical sciences investigating the relationship between cholesterol and Alzheimer's disease. SUMMARY: Cholesterol, its catabolites and proteins that regulate cholesterol levels all modulate processing of amyloid precursor protein. Statins hold promise in therapy of Alzheimer's disease, but the current data are more consistent with a model of statins that act as neuroprotective agents rather than inhibitors of beta-amyloid production.

Key concepts: Disease, Cholesterol, Dementia, Alzheimer's disease, Neuroprotection, Amyloid beta, Bioinformatics, Neuroscience

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