Cited by 61Alzheimer's disease research and treatmentsCholesterol and Lipid MetabolismDementia and Cognitive Impairment Research

Cholesterol metabolism, apolipoprotein E, adenosine triphosphate-binding cassette transporters, and Alzheimer's disease

Hirsch-Reinshagen, Veronica, Wellington, Cheryl L·2007·Current Opinion in Lipidology

Abstract

Purpose of review Recent evidence suggests that cholesterol metabolism participates in the pathogenesis of Alzheimer's disease. Apolipoprotein E is the main lipid carrier in the brain and the best-established risk factor for late-onset Alzheimer's disease. Intracellular cholesterol levels influence the generation of amyloid-beta peptides, the toxic species thought to be a primary cause of Alzheimer's disease. Finally, compounds that modulate cholesterol metabolism affect amyloid-beta generation. This review summarizes data linking apolipoprotein E and adenosine triphosphate-binding cassette transporters to aspects of cholesterol metabolism and Alzheimer's disease pathogenesis. Recent findings In vivo, the lipidation status of apolipoprotein E affects amyloid-beta burden in mice with Alzheimer's disease, which appears to caused by the modulation of amyloid-beta deposition or clearance rather than amyloid-beta production. State-of-the-art in-vivo assays reveal that amyloid-beta is cleared from the brain by multiple pathways. Members of the adenosine triphosphate-binding cassette superfamily of transporters regulate lipid homeostasis and apolipoprotein metabolism in the brain, and may affect Alzheimer's disease pathogenesis by modulating apolipoprotein E lipidation as well as intracellular sterol homeostasis. Summary Proteins involved in brain cholesterol metabolism may affect the pathogenesis of Alzheimer's disease. Compounds that modulate the expression of these proteins may b…

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Crossref · 10.1097/mol.0b013e32813aeabf

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89 of 89 references verified0 citation errors · 0 not checkable

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  • Previous in vitro and in vivo studies demonstrated that ABCA1 influences Aβ levels.

    “Previous in vitro and in vivo studies demonstrated that ABCA1 influences Aβ levels (Bu, 2009; Fan et al., 2009; Hirsch-Reinshagen and Wellington, 2007; Kim et al., 2009; Koldamova and Lefterov, 2007).”

    From miR-106b impairs cholesterol efflux and increases Aβ levels by repressing ABCA1 expression (2012) · cites this paper as Hirsch-Reinshagen and Wellington, 2007

  • Most previous studies suggested that the main mechanism by which ABCA1 affects extracellular Aβ level is through regulation of Aβ production, not through Aβ clearance.

    “Most previous studies suggested that the main mechanism by which ABCA1 affects extracellular Aβ level is through regulation of Aβ production, not through Aβ clearance (Di Paolo and Kim, 2011; Hirsch-Reinshagen and Wellington, 2007).”

    From miR-106b impairs cholesterol efflux and increases Aβ levels by repressing ABCA1 expression (2012) · cites this paper as Hirsch-Reinshagen and Wellington, 2007

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Authors
Hirsch-Reinshagen, V., & Wellington, C. L.
Affiliations
University of British Columbia (CA)
Corresponding author
Wellington, Cheryl L
Venue
Current Opinion in Lipidology
Published
2007-06
Volume
18
Issue
3
Pages
325-332
ISSN
0957-9672 (ISSN-L)
OpenAlex
W2030501070
Cited by
61
References
89
Citations by year
2024: 1 · 2023: 1 · 2022: 1 · 2021: 2 · 2020: 1 · 2019: 2 · 2018: 1 · 2017: 3 · 2016: 3 · 2015: 2 · 2014: 3 · 2013: 2 · 2012: 2
FWCI
1.11
Type
journal article
Language
en
Open access
closed
Locations
  • Current Opinion in Lipidology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
Alzheimer's disease, cholesterol metabolism, apolipoprotein E, ABC transporters, amyloid-beta clearance, amyloid-beta deposition, intracellular cholesterol, sterol homeostasis, lipid homeostasis, therapeutic target
MeSH terms
ATP Binding Cassette Transporter, Subfamily G, ATP Binding Cassette Transporter, Subfamily G, Member 1, Alzheimer Disease, Animals, Apolipoproteins E, Brain, Cholesterol, Homeostasis, Humans, Lipids, Models, Biological, Amyloid beta-Peptides, ATP-Binding Cassette Transporters, Lipid Metabolism, Mice

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