The DOI matches its Crossref record; 130 of the 131 references it cites were found in a registry or an index.
HDL and cholesterol handling in the brain
Abstract
Cholesterol is an essential component of both the peripheral nervous system and central nervous system (CNS) of mammals. Brain cholesterol is synthesized in situ by astrocytes and oligodendrocytes and is almost completely isolated from other pools of cholesterol in the body, but a small fraction can be taken up from the circulation as 27-hydroxycholesterol, or via the scavenger receptor class B type I. Glial cells synthesize native high-density lipoprotein (HDL)-like particles, which are remodelled by enzymes and lipid transfer proteins, presumably as it occurs in plasma. The major apolipoprotein constituent of HDL in the CNS is apolipoprotein E, which is produced by astrocytes and microglia. Apolipoprotein A-I, the major protein component of plasma HDL, is not synthesized in the CNS, but can enter and become a component of CNS lipoproteins. Low HDL-C levels have been shown to be associated with cognitive impairment and various neurodegenerative diseases. On the contrary, no clear association with brain disorders has been shown in genetic HDL defects, with the exception of Tangier disease. Mutations in a wide variety of lipid handling genes can result in human diseases, often with a neuronal phenotype caused by dysfunctional intracellular lipid trafficking.
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In the citing paper
“Therefore, cholesterol, HDL-like particles, and apolipoprotein E (ApoE) are synthesized in situ by glial cells [16–18].”
From Sterol and lipid analyses identifies hypolipidemia and apolipoprotein disorders in autism associated with adaptive functioning deficits (2021) · cites this paper as [18]
In the citing paper
“The transport of cholesterol from astrocytes to neurons occurs through peculiar lipoprotein particles, similar to plasma HDL [23]. Specifically, cholesterol and apoE newly produced by astrocytes are secreted and assembled in HDL-like particles which, after remodeling and maturation, finally deliver cholesterol to neurons through the apoE-recognizing receptors mentioned above [11,24].”
From PCSK9 affects astrocyte cholesterol metabolism and reduces neuron cholesterol supplying in vitro: potential implications in Alzheimer’s disease (2022) · cites this paper as [23]
In the citing paper
“In addition enhanced ApoE lipidation may prevent adverse effects of ApoE hypolipidation on neurodegeneration caused by insufficient cholesterol supply to neurons (Vitali et al., 2014).”
From ApoE4 Alters ABCA1 Membrane Trafficking in Astrocytes (2019) · cites this paper as Vitali et al., 2014
Citations
Cites
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Items 101–102 of 102
Cholesterol Metabolism in CNS Diseases: The Potential of SREBP2 and LXR as Therapeutic Targets
Wang, N.-Q., Sun, P.-X., Shen, Q.-Q., & Deng, M.-Y. (2025) · Molecular Neurobiology · doi:10.1007/s12035-024-04672-w · Cited by 19
Zhang, Y., Cheng, Z., Huang, S., Sharma, T., Barbosa, D., Yu, G., & Sun, L. O. (2025) · Cell Reports · doi:10.1016/j.celrep.2025.116252 · Cited by 4
Metadata
- Authors
- Vitali, C., Wellington, C. L., & Calabresi, L.
- Affiliations
- University of Milan (IT)
- University of British Columbia (CA)
- Corresponding author
- Calabresi, L.
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2014-06-06
- Volume
- 103
- Issue
- 3
- Pages
- 405-413
- ISSN
- 0008-6363 (ISSN-L)
- OpenAlex
- W2098990121
- Cited by
- 254
- References
- 131
- Citations by year
- 2026: 18 · 2025: 32 · 2024: 25 · 2023: 26 · 2022: 21 · 2021: 30 · 2020: 11 · 2019: 21 · 2018: 21 · 2017: 19 · 2016: 16 · 2015: 10 · 2014: 3
- FWCI
- 3.03
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cardiovascular Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- high-density lipoprotein, brain cholesterol, cholesterol metabolism, apolipoprotein E, apolipoprotein A-I, astrocytes, oligodendrocytes, microglia, 27-hydroxycholesterol, scavenger receptor class B type I, lipid transfer proteins, cognitive impairment, neurodegenerative diseases, Tangier disease, lipid trafficking, genetic lipid disorders
- MeSH terms
- Animals, Apolipoproteins, Brain, Humans, Cholesterol, HDL, Phenotype, Risk Factors, Neurodegenerative Diseases, Genetic Predisposition to Disease
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