Lipid Metabolism and Glial Lipoproteins in the Central Nervous System
Open accessAbstract
Lipoproteins in the central nervous system (CNS) are not incorporated from the blood but are formed mainly by glial cells within the CNS. In addition, cholesterol in the CNS is synthesized endogenously because the blood-brain barrier segregates the CNS from the peripheral circulation. Apolipoprotein (apo) E is a major apo in the CNS. In normal condition, apo E is secreted from glia, mainly from astrocytes, and forms cholesterol-rich lipoproteins by ATP-binding cassette transporters. Subsequently, apo E-containing glial lipoproteins supply cholesterol and other components to neurons via a receptor-mediated process. Recent findings demonstrated that receptors of the low density lipoprotein (LDL) receptor family not only internalize lipoproteins into the cells but also, like signaling receptors, transduce signals upon binding the ligands. In this review, the regulation of lipid homeostasis will be discussed as well as roles of lipoproteins and functions of receptors of LDL receptor family in the CNS. Furthermore, the relation between lipid metabolism and Alzheimer's disease (AD) is discussed.
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Astrocytes synthesize cholesterol at a higher rate than neurons and transfer excess cholesterol to neurons.
“strong evidence suggests that astrocytes synthesize cholesterol at a higher rate than neurons and transfer their excess cholesterol to neurons [38, 40].”
From MicroRNAs in brain cholesterol metabolism and their implications for Alzheimer's disease (2016) · cites this paper as [40]
Section 1 (Lipid Homeostasis in the CNS; page not available) says cholesterol synthesis after myelination occurs mainly in astrocytes, while neurons synthesize it inefficiently and obtain it from astrocytes. The paper supports transfer to neurons, but does not describe the cholesterol transferred as excess cholesterol in astrocytes. (LLM, conf=0.83)
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- Authors
- Hayashi, H.
- Affiliations
- Kumamoto University (JP)
- Corresponding author
- Hayashi, Hideki
- ORCID
- Hayashi, Hideki
- Venue
- Biological and Pharmaceutical Bulletin
- Publisher
- Pharmaceutical Society of Japan
- Published
- 2011
- Volume
- 34
- Issue
- 4
- Pages
- 453-461
- ISSN
- 0918-6158 (ISSN-L)
- 1347-5215
- OpenAlex
- W2132984653
- Cited by
- 80
- References
- 214
- Citations by year
- 2025: 2 · 2024: 6 · 2023: 5 · 2022: 4 · 2021: 3 · 2020: 6 · 2019: 3 · 2018: 3 · 2017: 5 · 2016: 7 · 2015: 6 · 2014: 11 · 2013: 7 · 2012: 10
- FWCI
- 1.73
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Biological and Pharmaceutical Bulletin (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ministry of Education, Culture, Sports, Science and Technology
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- Japan Society for the Promotion of Science (22790254)
- Topics
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- apolipoprotein E, astrocytes, cholesterol homeostasis, blood-brain barrier, ABC transporters, LDL receptor family, lipid metabolism, lipid homeostasis, Alzheimer's disease, central nervous system
- MeSH terms
- Alzheimer Disease, Animals, Apolipoproteins E, Central Nervous System, Cholesterol, Humans, Neuroglia, Neurons, Receptors, LDL, Signal Transduction, ATP-Binding Cassette Transporters, Lipid Metabolism
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