Central Nervous System Lipoproteins: ApoE and Regulation of Cholesterol Metabolism
Open accessAbstract
ApoE on high-density lipoproteins is primarily responsible for lipid transport and cholesterol homeostasis in the central nervous system (CNS). Normally produced mostly by astrocytes, apoE is also produced under neuropathologic conditions by neurons. ApoE on high-density lipoproteins is critical in redistributing cholesterol and phospholipids for membrane repair and remodeling. The 3 main structural isoforms differ in their effectiveness. Unlike apoE2 and apoE3, apoE4 has markedly altered CNS metabolism, is associated with Alzheimer disease and other neurodegenerative disorders, and is expressed at lower levels in brain and cerebrospinal fluid. ApoE4-expressing cultured astrocytes and neurons have reduced cholesterol and phospholipid secretion, decreased lipid-binding capacity, and increased intracellular degradation. Two structural features are responsible for apoE4 dysfunction: domain interaction, in which arginine-61 interacts ionically with glutamic acid-255, and a less stable conformation than apoE3 and apoE2. Blocking domain interaction by gene targeting (replacing arginine-61 with threonine) or by small-molecule structure correctors increases CNS apoE4 levels and lipid-binding capacity and decreases intracellular degradation. Small molecules (drugs) that disrupt domain interaction, so-called structure correctors, could prevent the apoE4-associated neuropathology by blocking the formation of neurotoxic fragments. Understanding how to modulate CNS cholesterol transport and metabolism is providing important insights into CNS health and disease.
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ApoE directly binds Aβ and, together with LDLR and LRP1, plays a key role in astrocyte-mediated Aβ clearance.
“Importantly, ApoE appeared to directly bind Aβ and, together with its receptors LDLR and LRP1, to play a key role in astrocyte-mediated Aβ clearance [27,28].”
From The Emerging Role of PCSK9 in the Pathogenesis of Alzheimer’s Disease: A Possible Target for the Disease Treatment (2024) · cites this paper as [27]
The section “Role of LDL Receptor Family Members in ApoE Delivery of Cholesterol to CNS Cells” identifies LDLR and LRP1 as receptors involved in apoE-mediated lipoprotein uptake by neurons and glia. “ApoE-Associated Neuropathology” discusses Aβ clearance only as a possible benefit of enhancing apoE4 lipidation and says it remains unproven. Neither passage establishes direct apoE–Aβ binding or a key role for these receptors in astrocyte-mediated Aβ clearance; page numbers are unavailable in our copy. (LLM, conf=0.83)
Experimental — accuracy not yet measuredThe presence of the blood-brain barrier requires cholesterol in the brain to be synthesized de novo, primarily by astrocytes.
“However, the presence of the blood–brain barrier requires cholesterol in the brain to be synthesized de novo, primarily by astrocytes (Jeske and Dietschy, 1980; Mahley, 2016).”
From Sterol dysregulation in Smith–Lemli–Opitz syndrome causes astrocyte immune reactivity through microglia crosstalk (2022) · cites this paper as Mahley, 2016
The Abstract says the blood–brain barrier restricts cholesterol entry and identifies astrocytes among the cells that synthesize CNS cholesterol. The ‘Cholesterol Synthesis and Metabolism in the CNS’ section says brain cholesterol is synthesized in situ and that adult production comes from glial cells and, to a lesser extent, neurons. Neither passage establishes that astrocytes specifically are the primary producers. (LLM, conf=0.86)
Experimental — accuracy not yet measuredApoE is a central apolipoprotein in cerebral cholesterol metabolism and is involved in brain amyloid metabolism, blood brain barrier integrity, and transport of various lipid species to neuronal cells.
“apoE is a central apolipoprotein in cerebral cholesterol metabolism and is involved in brain amyloid metabolism, blood brain barrier integrity, and transport of various lipid species to neuronal cells [15][16][17][18][19].”
From APOE and vascular disease: Sequencing and genotyping in general population cohorts (2023) · cites this paper as [15]
The Abstract identifies apoE as critical to CNS cholesterol and lipid transport, and “ApoE4 Structure Targets It for Degradation and Decreased Lipid Transport” says it delivers cholesterol and phospholipid to neurons. “ApoE-Associated Neuropathology” links apoE4 to amyloid deposition, but describes a proposed role in Aβ clearance as unproven. The passages on the blood–brain barrier describe its restriction of lipid movement, not a role for apoE in maintaining barrier integrity. (LLM, conf=0.88)
Experimental — accuracy not yet measuredApoE4 association with lower ApoE level is more likely due to misfolding and accumulation of ApoE protein in the endoplasmic reticulum from an ionic interaction between Arg-61 in the N-terminal domain and Glu-255 in the C-terminal domain in the E4 isoform; this domain interaction is not present in the other two ApoE isoforms.
“ii) more likely, it is the result of misfolding and accumulation of ApoE protein in endoplasmic reticulum due to an ionic interaction between Arg-61 in the N-terminal domain and Glu-255 in the C-terminal domain in the E4 isoform; this domain interaction is not present in the other two ApoE isoforms [3, 4].”
From Genome-wide analysis identifies novel loci influencing plasma apolipoprotein E concentration and Alzheimer’s disease risk (2023) · cites this paper as [3]
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredApoE is the major cholesterol carrier in the central nervous system; in the brain, lipids are transported on HDL-like particles where apoE is the primary apolipoprotein, unlike in the circulation where apoA1 is primary and apoE is present at lower levels.
“ApoE is the major cholesterol carrier in the central nervous system: in the brain, lipids are transported on lipoproteins that resemble HDL particles, but while apolipoprotein A1 (apoA1) is the primary apolipoprotein and apoE is present in lower levels in HDL in the circulation, in contrast apoE is the primary apolipoprotein on these HDL-like particles found in the brain [67,73,75].”
From Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review (2016) · cites this paper as [75]
The level of apoE in cerebrospinal fluid has been estimated to be about 10-20% of the level in plasma.
“The level of apoE in cerebrospinal fluid has been estimated to ~10e20% of the level in plasma [75].”
From Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review (2016) · cites this paper as [75]
Proteinaceous lipid nanoparticles (LNPs) are the main vehicles for lipid transport between cells in mammals.
“Proteinaceous lipid nanoparticles (LNPs) are the main vehicles for lipid transport between cells in mammals.1–4”
From ApoE is Secreted as a Lipid Nanoparticle by Mammalian Cells: Implications for Alzheimer’s Disease Pathogenesis (2025) · cites this paper as [3]
ApoE2 association with high ApoE level is due to its decreased binding with LDL receptor, resulting in higher plasma level.
“In the APOE region, association of ApoE2 with high ApoE level is due to its decreased binding with LDL receptor, resulting in higher plasm level.”
From Genome-wide analysis identifies novel loci influencing plasma apolipoprotein E concentration and Alzheimer’s disease risk (2023) · cites this paper as [3]
APOE aids in cholesterol and lipid efflux from the cell by associating with lipoprotein particles upon formation.
“In turn, APOE aids in cholesterol and lipid efflux from the cell by associating with lipoprotein particles upon formation (Mahley, 2016).”
From APOE2, E3, and E4 differentially modulate cellular homeostasis, cholesterol metabolism, and inflammatory response in isogenic iPSC-derived astrocytes (2022) · cites this paper as Mahley, 2016
These results demonstrate an isoform-dependent regulation of APOE protein levels, as previously shown for E3 and E4 in vitro or in patient CSF.
“These results demonstrate an isoform-dependent regulation of APOE protein levels, as was previously shown for E3 and E4 in vitro, or in patient cerebrospinal fluid (CSF) (Lin et al., 2018; Mahley, 2016).”
From APOE2, E3, and E4 differentially modulate cellular homeostasis, cholesterol metabolism, and inflammatory response in isogenic iPSC-derived astrocytes (2022) · cites this paper as Mahley, 2016
Astrocyte-derived ApoE is important for cholesterol transport through ApoE-containing 'HDL-like' particles, which play an important role in synaptic development and maintenance.
“Astrocyte-derived ApoE is important for cholesterol transport through ApoE-containing “HDL-like” particles, which play an important role in synaptic development and maintenance [1, 4, 5].”
From ApoE, ApoE Receptors, and the Synapse in Alzheimer's Disease (2017) · cites this paper as [5]
A major role of APOE is to facilitate the transport of cholesterol from astrocytes to neurons in the CNS.
“a major role of APOE is to facilitate the transport of cholesterol from astrocytes to neurons in the CNS [188].”
From Genetic architecture of Alzheimer's disease (2020) · cites this paper as [188]
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“Several factors implicate cholesterol metabolism in the pathogenesis of AD; a major role of APOE is to facilitate the transport of cholesterol from astrocytes to neurons in the CNS (Mahley, 2016).”
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“However, the presence of the blood – brain barrier requires cholesterol in the brain to be synthesized de novo , primarily by astrocytes (Jeske and Dietschy, 1980; Mahley, 2016).”
APOE4 Increases Energy Metabolism in APOE-Isogenic iPSC-Derived Neurons
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“Importantly, ApoE appeared to directly bind A β and, together with its receptors LDLR and LRP1, to play a key role in astrocyte-mediated A β clearance [27,28].”
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- Authors
- Mahley, R. W.
- Affiliations
- University of California, San Francisco (US)
- Corresponding author
- Mahley, Robert W.
- ORCID
- Mahley, Robert W.
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 2016-07
- Volume
- 36
- Issue
- 7
- Pages
- 1305-1315
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- PMC
- PMC4942259
- OpenAlex
- W2560393860
- Cited by
- 516
- References
- 113
- Citations by year
- 2026: 55 · 2025: 78 · 2024: 51 · 2023: 66 · 2022: 72 · 2021: 64 · 2020: 48 · 2019: 31 · 2018: 22 · 2017: 25 · 2016: 4
- FWCI
- 21.98
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- Wellcome Trust (101786)
- National Institute on Aging (R01AG028793)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Keywords
- apolipoprotein E, APOE ε4, APOE isoforms, high-density lipoprotein, cholesterol homeostasis, astrocytes, neurons, membrane lipid remodeling, Alzheimer's disease, domain interactions, neurodegenerative diseases, cerebrospinal fluid
- MeSH terms
- Alzheimer Disease, Animals, Apolipoproteins E, Astrocytes, Biological Transport, Central Nervous System, Cholesterol, Humans, Nerve Degeneration, Neurons, Protein Binding, Neurodegenerative Diseases, Models, Animal, Protein Interaction Domains and Motifs
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