Journal
MOLECULAR NEUROBIOLOGY
Volume 47, Issue 1, Pages 37-63Publisher
SPRINGER
DOI: 10.1007/s12035-012-8337-y
Keywords
beta-Amyloid peptide; Neurotoxicity; Lipid rafts; Neuronal cholesterol level/distribution
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Funding
- Canadian Institutes of Health Research
- Alberta Innovates Health Research Studentship Award
- Canada Research Chairs
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Alzheimer's disease (AD) is a complex multifactorial neurodegenerative disorder believed to be initiated by accumulation of amyloid beta (A beta)-related peptides derived from proteolytic processing of amyloid precursor protein (APP). Research over the past two decades provided a mechanistic link between cholesterol and AD pathogenesis. Genetic polymorphisms in genes regulating the pivotal points in cholesterol metabolism have been suggested to enhance the risk of developing AD. Altered neuronal membrane cholesterol level and/or subcellular distribution have been implicated in aberrant formation, aggregation, toxicity, and degradation of A beta-related peptides. However, the results are somewhat contradictory and we still do not have a complete understanding on how cholesterol can influence AD pathogenesis. In this review, we summarize our current understanding on the role of cholesterol in regulating the production/function of A beta-related peptides and also examine the therapeutic potential of regulating cholesterol homeostasis in the treatment of AD pathology.
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