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Biomed Res Int. 2013;2013:814390. doi: 10.1155/2013/814390. Epub 2014 Feb 19.

The impact of cholesterol, DHA, and sphingolipids on Alzheimer's disease.

Author information

1
Experimental Neurology, Saarland University, Kirrberger Street 1, 66421 Homburgr, Saar, Germany ; Neurodegeneration and Neurobiology, Saarland University, Kirrberger Street 1, 66421 Homburg, Germany ; Deutsches Institut für DemenzPrävention (DIDP), Saarland University, Kirrberger Street 1, 66421 Homburgr, Saar, Germany.
2
Experimental Neurology, Saarland University, Kirrberger Street 1, 66421 Homburgr, Saar, Germany.

Abstract

Alzheimer's disease (AD) is a devastating neurodegenerative disorder currently affecting over 35 million people worldwide. Pathological hallmarks of AD are massive amyloidosis, extracellular senile plaques, and intracellular neurofibrillary tangles accompanied by an excessive loss of synapses. Major constituents of senile plaques are 40-42 amino acid long peptides termed β -amyloid (A β ). A β is produced by sequential proteolytic processing of the amyloid precursor protein (APP). APP processing and A β production have been one of the central scopes in AD research in the past. In the last years, lipids and lipid-related issues are more frequently discussed to contribute to the AD pathogenesis. This review summarizes lipid alterations found in AD postmortem brains, AD transgenic mouse models, and the current understanding of how lipids influence the molecular mechanisms leading to AD and A β generation, focusing especially on cholesterol, docosahexaenoic acid (DHA), and sphingolipids/glycosphingolipids.

PMID:
24575399
PMCID:
PMC3929518
DOI:
10.1155/2013/814390
[Indexed for MEDLINE]
Free PMC Article

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