Abstract |
This article puts forward the hypothesis that the Low Density Lipid Receptor (LDLR) is one of the molecules that is involved in the clearance of amyloid proteins in the brain and that it may play a role in Alzheimer's Disease (AD) via its up-regulation by statins. The hypothesis is built on the following observations: a- statins (which have been shown to increase LDLR in astrocytes, see below) have a beneficial role in AD, b-defects in the LDL receptor gene are found in AD, c-molecules with similar structure to the LDLR have been shown to clear amyloid protein from the brain.
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Authors | Yasir Abdulkarim, Zeyad Hameed |
Journal | Neurochemical research
(Neurochem Res)
Vol. 31
Issue 6
Pg. 839-47
(Jun 2006)
ISSN: 0364-3190 [Print] United States |
PMID | 16841190
(Publication Type: Journal Article, Review)
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Chemical References |
- Amyloid beta-Peptides
- Amyloid beta-Protein Precursor
- Hydroxymethylglutaryl-CoA Reductase Inhibitors
- Receptors, LDL
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Topics |
- Alzheimer Disease
(drug therapy)
- Amyloid beta-Peptides
(metabolism)
- Amyloid beta-Protein Precursor
(metabolism)
- Female
- Humans
- Hydroxymethylglutaryl-CoA Reductase Inhibitors
(therapeutic use)
- Male
- Polymorphism, Genetic
- Prospective Studies
- Receptors, LDL
(genetics, physiology)
- Retrospective Studies
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