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Cited by 1,166

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Cholesterol depletion inhibits the generation of β-amyloid in hippocampal neurons

Open access
Simons, Mikael, Keller, Patrick, De Strooper, Bart, Beyreuther, Konrad, Dotti, Carlos G., Simons, Kai·1998·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.95.11.6460
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Abstract

The amyloid precursor protein (APP) plays a crucial role in the pathogenesis of Alzheimer’s disease. During intracellular transport APP undergoes a series of proteolytic cleavages that lead to the release either of an amyloidogenic fragment called β-amyloid (Aβ) or of a nonamyloidogenic secreted form consisting of the ectodomain of APP (APP sec ). It is Aβ that accumulates in the brain lesions that are thought to cause the disease. By reducing the cellular cholesterol level of living hippocampal neurons by 70% with lovastatin and methyl-β-cyclodextrin, we show that the formation of Aβ is completely inhibited while the generation of APP sec is unperturbed. This inhibition of Aβ formation is accompanied by increased solubility in the detergent Triton X-100 and is fully reversible by the readdition of cholesterol to previously depleted cells. Our results show that cholesterol is required for Aβ formation to occur and imply a link between cholesterol, Aβ, and Alzheimer’s disease.

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Metadata

Authors
Simons, M., Keller, P., De Strooper, B., Beyreuther, K., Dotti, C. G., & Simons, K.
Venue
Proceedings of the National Academy of Sciences
Publisher
Proceedings of the National Academy of Sciences
Published
1998-05-26
Volume
95
Issue
11
Pages
6460-6464
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
DOI
10.1073/pnas.95.11.6460
OpenAlex
W1975806945
Cited by
1,166
References
3
FWCI
24.09
Type
journal article
Language
en
Open access
green

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