Apolipoprotein E4 Alters Astrocyte Fatty Acid Metabolism and Lipid Droplet Formation
Open accessAbstract
Lipid droplets (LDs) serve as energy rich reservoirs and have been associated with apolipoprotein E (APOE) and neurodegeneration. The E4 allele of APOE (E4) is the strongest genetic risk factor for the development of late onset Alzheimer’s disease (AD). Since both E4 carriers and individuals with AD exhibit a state of cerebral lipid dyshomeostasis, we hypothesized that APOE may play a role in regulating LD metabolism. We found that astrocytes expressing E4 accumulate significantly more and smaller LDs compared to E3 astrocytes. Accordingly, expression of perilipin-2, an essential LD protein component, was higher in E4 astrocytes. We then probed fatty acid (FA) metabolism and found E4 astrocytes to exhibit decreased uptake of palmitate, and decreased oxidation of exogenously supplied oleate and palmitate. We then measured oxygen consumption rate, and found E4 astrocytes to consume more oxygen for endogenous FA oxidation and accumulate more LD-derived metabolites due to incomplete oxidation. Lastly, we found that E4 astrocytes are more sensitive to carnitine palmitoyltransferase-1 inhibition than E3 astrocytes. These findings offer the potential for further studies investigating the link between astrocyte lipid storage, utilization, and neurodegenerative disease as a function of APOE genotype.
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Increased lipid droplet accumulation in ApoE4-expressing astrocytes has been thought to result from dysregulation of lipid homeostasis in neuroinflammation.
“Increased LD accumulation in ApoE4-expressing astrocytes has been thought to result from the dysregulation of lipid homeostasis in neuroinflammation (20)(21)(22).”
From Regulation of astrocyte lipid metabolism and ApoE secretion by the microglial oxysterol, 25-hydroxycholesterol (2023) · cites this paper as [20]
The Conclusions (Section 5; page unavailable) report more lipid droplets and altered fatty-acid metabolism in E4 astrocytes than in E3 astrocytes. The paper does not establish that neuroinflammation causes the increased accumulation, so that explanation is not supported. (LLM, conf=0.88)
Experimental — accuracy not yet measuredAPOE4 astrocytes have an increased number of lipid droplets and impaired glucose utilization and mitochondrial function.
“APOE4 astrocytes have an increased number of lipid droplets and impaired glucose utilization and mitochondrial function, lending further support to this hypothesis143,146,147 (Fig. 2b).”
From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [146]
The Conclusions report more lipid droplets in E4 than E3 astrocytes and altered fatty-acid oxidation. Results §3.3 reports lower oxygen consumption in E4 astrocytes, but only suggests that reduced glucose oxidation is the likely cause; it does not establish impaired glucose utilization or mitochondrial function generally. (LLM, conf=0.86)
Experimental — accuracy not yet measuredGlial cells store excess free fatty acids as triglycerides and cholesterol esters in intracellular lipid droplets, which are catabolized in mitochondria via β-oxidation, and this process is compromised in the presence of APOE4.
“Glial cells then store excess free fatty acids in the form of triglycerides and cholesterol esters in intracellular lipid droplets, which serve as an energy storage until they are catabolized in mitochondria via β-oxidation, and this process is compromised in the presence of APOE4 (refs. 146,177)”
From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [146]
The Introduction describes lipid droplets as containing triacylglycerols and cholesterol esters, and the Discussion says astrocyte lipid droplets sequester fatty acids and provide an energy reservoir. Results §3.3 shows that APOE4 alters fatty-acid oxidation in astrocytes, but not as a uniform reduction in catabolism of stored lipids: E4 astrocytes had higher oxygen consumption attributed to endogenous fatty-acid oxidation and no difference in CO2 production from intracellular fatty acids. The claim's broad description of this process as ‘compromised’ therefore misses the distinction between stored and externally supplied fatty acids. (LLM, conf=0.87)
Experimental — accuracy not yet measuredAPOE4 astrocytes accumulate unsaturated triglycerides in lipid droplets in both mouse and human iPSC-derived astrocytes.
“APOE4 astrocytes accumulate unsaturated triglycerides in lipid droplets in both mouse15,16 and human iPSC-derived astrocytes24,30.”
From APOE genotypes differentially remodel the astrocytic lipid droplet proteome to shape lipid droplet dynamics (2026) · cites this paper as [15]
The Methods (§2.1) identify the studied astrocytes as mouse-derived, and the Results (§3.1) show that APOE4 cells had more lipid droplets than APOE3 cells. The paper does not establish that the accumulated droplets specifically contain unsaturated triglycerides. Its own experiments also do not use human iPSC-derived astrocytes, though the citing sentence attaches other citations to that portion. (LLM, conf=0.87)
Experimental — accuracy not yet measuredAltered lipid droplet biology has been linked to both brain aging and neurodegenerative diseases.
“Altered lipid droplet biology has been linked to both brain aging and neurodegenerative diseases10–24.”
From APOE genotypes differentially remodel the astrocytic lipid droplet proteome to shape lipid droplet dynamics (2026) · cites this paper as [15]
The Introduction reports increased lipid-droplet content in Parkinson’s disease and Alzheimer’s disease, supporting the neurodegenerative-disease link. The passages found do not establish a link between altered lipid-droplet biology and brain aging; the References list a study of lipid-laden cells in the aging brain, but the paper does not state that broader claim. (LLM, conf=0.82)
Experimental — accuracy not yet measured
APOE has an isoform-specific impact on lipid droplet accumulation in astrocytes, neurons and microglia.
“Work both in vitro and in vivo has highlighted an APOE isoform-specific impact on lipid droplet accumulation in astrocytes146, neurons177 and microglia178.”
From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [146]
Mouse astrocytes expressing human APOE4 have defects in lipid droplet metabolism as well as in fatty acid uptake and oxidation.
“Mouse astrocytes expressing human APOE4 have defects in LD metabolism as well as in fatty acid uptake and oxidation (Farmer et al., 2019; Qi et al., 2021).”
From APOE traffics to astrocyte lipid droplets and modulates triglyceride saturation and droplet size (2024) · cites this paper as Farmer et al., 2019
E4-expressing astrocytes and E4 microglia accumulate more lipid droplets than E3-expressing cells.
“E4 expressing astrocytes (Windham et al., 2024; Farmer et al., 2019; Sienski et al., 2021) and E4 microglia (Machlovi et al., 2022; Victor et al., 2022; Haney et al., 2024) both accumulate more lipid droplets than neutral AD-risk ε3/ε3 (E3) expressing cells.”
From APOE4 reshapes the lipid droplet proteome and modulates microglial inflammatory responses (2025) · cites this paper as Farmer et al., 2019
Astrocytic lipid droplets accumulate in an APOE genotype-dependent manner.
“Astrocytic lipid droplets also accumulate in an APOE genotype-dependent manner.”
From APOE genotypes differentially remodel the astrocytic lipid droplet proteome to shape lipid droplet dynamics (2026) · cites this paper as [15]
Studies in various model systems have linked APOE4 with increased astrocytic lipid droplets.
“studies in various model systems have linked APOE4 with increased astrocytic lipid droplets15,16,20,24.”
From APOE genotypes differentially remodel the astrocytic lipid droplet proteome to shape lipid droplet dynamics (2026) · cites this paper as [15]
The effects of APOE on the composition of lipid droplets themselves remain unexplored.
“the effects of APOE on the composition of LDs themselves remains unexplored”
From APOE4 reshapes the lipid droplet proteome and modulates microglial inflammatory responses (2025) · cites this paper as Farmer et al., 2019
The Discussion says the link between E4 and lipid-droplet biology had not been widely explored, but does not identify droplet composition as an unexplored question. The Results examine droplet number, size, volume, and perilipin-2 expression; the passages found do not establish whether APOE’s effects on the composition of droplets themselves had been studied. (LLM, conf=0.70)
Experimental — accuracy not yet measured
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“Lipid accumulation in AD has been under-studied relative to other pathologies, but alterations in lipid metabolism and homeostasis are now emerging as a hallmark of AD brains (Liu and Zhang, 2014; Farmer et al., 2019; Wong et al., 2017).”
BackgroundLipid metabolism in astrocytic structure and function
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Self-citation
- Authors
- Farmer, B., Kluemper, J., & Johnson, L.
- Affiliations
- University of Kentucky (US)
- Corresponding author
- Johnson, Lance
- Venue
- Cells
- Publisher
- MDPI AG
- Published
- 2019-02-20
- Volume
- 8
- Issue
- 2
- Pages
- 182
- ISSN
- 2073-4409 (ISSN-L)
- PMC
- PMC6406677
- OpenAlex
- W2917914009
- Cited by
- 164
- References
- 62
- Citations by year
- 2026: 12 · 2025: 29 · 2024: 23 · 2023: 23 · 2022: 28 · 2021: 21 · 2020: 21 · 2019: 6
- FWCI
- 8.04
- Type
- journal article
- Language
- en
- Open access
- gold
- dx.doi.org
- Licence
- Locations
- Cells (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- UKnowledge (University of Kentucky) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- American Heart Association (19PRE34380094)
- National Institute on Aging (1R01AG060056-01)
- National Institutes of Health (P20 GM103527)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
- Keywords
- APOE ε4, astrocytes, lipid droplets, fatty acid metabolism, lipid droplet formation, PLIN2, palmitate uptake, fatty acid oxidation, oxygen consumption, carnitine palmitoyltransferase 1, Alzheimer's disease, neurodegeneration
- MeSH terms
- Animals, Astrocytes, Carnitine O-Palmitoyltransferase, Fatty Acids, Humans, Oxidation-Reduction, Oleic Acid, Palmitic Acid, Mice, Apolipoprotein E4, Lipid Droplets
About these checks
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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