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Lipid Alterations in the Earliest Clinically Recognizable Stage of Alzheimers Disease: Implication of the Role of Lipids in the Pathogenesis of Alzheimers Disease
Abstract
Lipids have many important yet distinct functions in cellular homeostasis such as forming an impermeable barrier separating intracellular and extracellular compartments, providing a matrix for the appropriate interactions of membrane-associated proteins, and serving as storage reservoirs for biologically active second messengers. Alterations in cellular lipids may therefore result in abnormal cellular functions. This review summarizes the results from the examination of lipid alterations in Alzheimer's disease (AD). In addition to the effects of cholesterol on AD, substantial depletions of plasmalogen and sulfatide as well as dramatic increases in ceramide are specifically manifested at the earliest clinically recognizable stage of AD. The potential mechanism(s) underlying these changes and the potential consequences of these changes in neuronal function and in AD development are also discussed. Collectively, this review will provide an overview of the lipid alterations in Alzheimer's disease and the relationship of these lipid alterations with the development of AD pathogenesis.
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“Notably, previous studies have shown that the lipids that were or tended to be decreased in PLCG2 KO mice (cerebrosides, sulfatides and plasmalogens) have been also reported to be decreased early in AD (39–41).”
From Multi-omics analyses reveal novel effects of PLCγ2 deficiency in the mouse brain (2023) · cites this paper as [40]
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Butyrylcholinesterase genotype and gender influence Alzheimer's disease phenotype
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Self-citationIslam, M. S., Castellucci, C., Fiorini, R., Greco, S., Gagliardi, R., Zannotti, A., Giannubilo, S. R., Ciavattini, A., Frega, N. G., Pacetti, D., et al. (2018) · Journal of Cellular Physiology · doi:10.1002/jcp.26537 · Cited by 28
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Metadata
- Authors
- Han, X.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Han, Xianlin
- ORCID
- Han, Xianlin
- Venue
- Current Alzheimer Research
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2005-01-01
- Volume
- 2
- Issue
- 1
- Pages
- 65-77
- ISSN
- 1567-2050 (ISSN-L)
- OpenAlex
- W1986724957
- Cited by
- 183
- References
- 146
- Citations by year
- 2026: 1 · 2025: 11 · 2024: 8 · 2023: 10 · 2022: 13 · 2021: 12 · 2020: 8 · 2019: 10 · 2018: 8 · 2017: 8 · 2016: 4 · 2015: 9 · 2014: 9 · 2013: 10 · 2012: 12
- FWCI
- 5.42
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Alzheimer Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (P01 AG0 3991, P01AG003991)
- National Heart, Lung, and Blood Institute (P01HL57278, P01HL057278)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Sphingolipid Metabolism and Signaling
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, lipid changes, cholesterol, plasmalogens, sulfatide, ceramide, Alzheimer's disease pathogenesis, neuronal function, membrane lipids
- MeSH terms
- Alzheimer Disease, Apolipoproteins E, Ceramides, Cholesterol, Humans, Plasmalogens, Sulfoglycosphingolipids
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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