Cholesterol and matrisome pathways dysregulated in astrocytes and microglia
Open accessAbstract
The impact of apolipoprotein E ε4 (APOE4), the strongest genetic risk factor for Alzheimer's disease (AD), on human brain cellular function remains unclear. Here, we investigated the effects of APOE4 on brain cell types derived from population and isogenic human induced pluripotent stem cells, post-mortem brain, and APOE targeted replacement mice. Population and isogenic models demonstrate that APOE4 local haplotype, rather than a single risk allele, contributes to risk. Global transcriptomic analyses reveal human-specific, APOE4-driven lipid metabolic dysregulation in astrocytes and microglia. APOE4 enhances de novo cholesterol synthesis despite elevated intracellular cholesterol due to lysosomal cholesterol sequestration in astrocytes. Further, matrisome dysregulation is associated with upregulated chemotaxis, glial activation, and lipid biosynthesis in astrocytes co-cultured with neurons, which recapitulates altered astrocyte matrisome signaling in human brain. Thus, APOE4 initiates glia-specific cell and non-cell autonomous dysregulation that may contribute to increased AD risk.
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APOE4 increases cholesterol sequestration in astrocytes leading to changes in the brain matrisome.
“and increases cholesterol sequestration in astrocytes leading to changes in the brain matrisome11.”
From APOE4 impairs myelination via cholesterol dysregulation in oligodendrocytes (2022) · cites this paper as [11]
The Results section, “Matrisome exacerbates lipid dysregulation in APOE4 astrocytes” (page unavailable), states that APOE4 drives lysosomal cholesterol sequestration in astrocytes and that matrisome dysregulation occurs. It does not say sequestration leads to matrisome changes; instead, it links those changes partly to astrocyte–neuron communication and says they worsen lipid dysregulation. (LLM, conf=0.88)
Experimental — accuracy not yet measuredFilipin only stains free (unesterified) cholesterol, and cellular cholesterol accumulation is associated with excess LD.
“Although filipin only stains free (unesterified) cholesterol, cellular cholesterol accumulation is associated with excess LD10,37,38.”
From PICALM Alzheimer’s risk allele causes aberrant lipid droplets in microglia (2025) · cites this paper as [38]
The Results section ('Impaired cholesterol trafficking in APOE4 astrocytes and microglia'; page unavailable) identifies filipin as a measure of intracellular free cholesterol, supporting the first part of the claim. The Discussion mentions lipid-droplet accumulation only while describing another study's finding about choline deficiency and unsaturated fatty acids; it does not establish an association between cellular cholesterol accumulation and excess lipid droplets. (LLM, conf=0.87)
Experimental — accuracy not yet measuredCholesterol-rich lysosomes and lipid droplets in dysfunctional microglia have been observed in demyelination mouse models and human iPS cell models.
“Cholesterol-rich lysosomes and LDs in dysfunctional microglia have also been observed in the context of demyelination mouse models and human iPS cell models9–12.”
From APOE4/4 is linked to damaging lipid droplets in Alzheimer’s disease microglia (2024) · cites this paper as [12]
The Results (‘Altered lipid metabolism in human APOE4 microglia and astrocytes’; page unavailable) report impaired cholesterol metabolism in human iPSC-derived microglia and predict lysosomal cholesterol accumulation. They do not establish cholesterol-rich lysosomes or lipid droplets in those microglia, or report those observations in demyelination mouse models. The measured increase in lysosomal cholesterol described in ‘Impaired cholesterol trafficking’ was in astrocytes. (LLM, conf=0.84)
Experimental — accuracy not yet measuredIn disease models, ApoE4 perturbs cholesterol regulation, including expression of cholesterol metabolism-related genes, cholesterol transport and esterification.
“In disease models, ApoE4 perturbs cholesterol regulation, including expression of cholesterol metabolism-related genes, cholesterol transport and esterification10–13.”
From Decreased lipidated ApoE‐receptor interactions confer protection against pathogenicity of ApoE and its lipid cargoes in lysosomes (2025) · cites this paper as [13]
The Results sections on altered lipid metabolism and impaired cholesterol trafficking report APOE4-related changes in cholesterol-metabolism gene expression, transporters, and efflux in astrocytes and microglia. They do not establish perturbed cholesterol esterification: the measured increase in astrocyte cholesterol came from free cholesterol, not cholesteryl esters. Page numbers were not available in our copy. (LLM, conf=0.90)
Experimental — accuracy not yet measuredMicroglia cholesterol synthesis plays a critical role in promoting normal microglia function.
“Our work, which suggests a critical role for microglia cholesterol synthesis in promoting normal microglia function, agrees with recently published work in multiple sclerosis and Alzheimer's disease (Berghoff et al., 2021; Tcw et al., 2022).”
From Sterol dysregulation in Smith–Lemli–Opitz syndrome causes astrocyte immune reactivity through microglia crosstalk (2022) · cites this paper as Tcw et al., 2022
The Results section on impaired cholesterol trafficking reports altered cholesterol synthesis in APOE4 microglia and reduced myelin uptake, a microglial function. The Discussion also links microglial lipid dysregulation to impaired debris recycling and inflammation. These findings support a connection between cholesterol metabolism and microglial function, but do not establish that cholesterol synthesis itself is critical for promoting normal function. (LLM, conf=0.83)
Experimental — accuracy not yet measured
Astrocytes derived from APOE4 human-inducible pluripotent stem cells are less efficient at secreting lipidated APOE particles and exhibit impaired cholesterol metabolism relative to APOE3 hiPSC-derived astrocytes.
“Astrocytes derived from APOE4 human-inducible pluripotent stem cells (hiPSCs) are less efficient at secreting lipidated APOE particles and exhibit impaired cholesterol metabolism relative to APOE3 hiPSC-derived astrocytes143,144.”
From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [144]
The Results section, “Impaired cholesterol trafficking in APOE4 astrocytes and microglia” (page unavailable), reports 63% less secreted APOE in APOE4 than APOE3 astrocytes, along with increased cellular cholesterol and reduced cholesterol efflux. The study used hiPSC-derived astrocytes, but the cited passages do not establish that the secreted APOE was lipidated or measure secretion of lipidated APOE particles specifically. (LLM, conf=0.86)
Experimental — accuracy not yet measuredRecent studies on human induced pluripotent stem cells with the APOE4 variant showed altered transcriptomic and metabolomic profiles toward the accumulation of cholesterol in glia, such as astrocytes and oligodendrocytes.
“Recent studies on human induced pluripotent stem cells (iPSCs) with the APOE4 variant showed altered transcriptomic and metabolomic profiles toward the accumulation of cholesterol in glia, such as astrocytes and oligodendrocytes.5”
From ApoE4-dependent lysosomal cholesterol accumulation impairs mitochondrial homeostasis and oxidative phosphorylation in human astrocytes (2023) · cites this paper as [7]
The Results sections on altered lipid metabolism and impaired cholesterol trafficking report APOE4-associated transcriptomic changes and increased intracellular cholesterol in hiPSC-derived astrocytes, supported by cholesterol measurements. The paper studies astrocytes and microglia, not oligodendrocytes, and the cited passages do not establish altered metabolomic profiles across glial cell types. Page numbers are unavailable in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIn vitro studies show APOE genetic variation can alter cellular metabolic profiles in distinct cell types including astrocytes, microglia, and neurons.
“Studies performed in vitro have shown that APOE genetic variation can alter cellular metabolic profiles in distinct cell types including astrocytes, microglia, and neurons [27][28][29][30] .”
From APOE4-drives brain bioenergetic shifts independent of Alzheimer’s disease pathology (2026) · cites this paper as [29]
The Introduction and Results (‘Altered lipid metabolism in human APOE4 microglia and astrocytes’; page unavailable) report APOE4-related lipid metabolic changes in in-vitro astrocytes and microglia. The paper also studies mixed neuron–astrocyte cultures and discusses a prior finding on cholesterol efflux in rat neurons, but it does not establish a distinct neuronal metabolic profile in its own experiments. (LLM, conf=0.84)
Experimental — accuracy not yet measuredMultiple transcriptomic studies of APOE4-expressing iPSC-derived astrocytes and microglia demonstrate alterations in expression of lipid metabolic genes and defects in cholesterol trafficking and metabolism.
“Multiple transcriptomic studies of APOE4-expressing iPSC-derived astrocytes and microglia demonstrate alterations in the expression of lipid metabolic genes as well as defects in cholesterol trafficking and metabolism (Lin et al., 2018; de Leeuw et al., 2022; Tcw et al., 2022).”
From APOE traffics to astrocyte lipid droplets and modulates triglyceride saturation and droplet size (2024) · cites this paper as Tcw et al., 2022
Observations of reduced APOE levels have been previously reported by other groups.
“Observations of reduced APOE levels have been previously reported by other groups 29,31 .”
From APOE4-drives brain bioenergetic shifts independent of Alzheimer’s disease pathology (2026) · cites this paper as [29]
Differences in lipid metabolism exist between APOE mouse and human models.
“Given differences in lipid metabolism between APOE mouse and human models37, we chose to investigate this question in human iPSC-derived astrocytes.”
From APOE genotypes differentially remodel the astrocytic lipid droplet proteome to shape lipid droplet dynamics (2026) · cites this paper as [37]
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- Authors
- TCW, J., Qian, L., Pipalia, N. H., Chao, M. J., Liang, S. A., Shi, Y., Jain, B. R., Bertelsen, S. E., Kapoor, M., Marcora, E., Sikora, E., Andrews, E. J., Martini, A. C., Karch, C. M., Head, E., Holtzman, D. M., Zhang, B., Wang, M., Maxfield, F. R., Poon, W. W., & Goate, A. M.
- Affiliations
- Boston University (US)
- Weill Cornell Medicine (US)
- Icahn School of Medicine at Mount Sinai (US)
- University of California, Irvine (US)
- Washington University in St. Louis (US)
- Regeneron (United States) (US)
- Corresponding author
- TCW, Julia
- Goate, Alison M.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2022-06
- Volume
- 185
- Issue
- 13
- Pages
- 2213-2233.e25
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC9340815
- OpenAlex
- W4283360267
- Cited by
- 411
- References
- 130
- Citations by year
- 2026: 93 · 2025: 101 · 2024: 95 · 2023: 79 · 2022: 37 · 2021: 4 · 2019: 1
- FWCI
- 50.10
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 388 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- Pfizer
- National Center for Research Resources (1S10RR025496-01)
- National Heart, Lung, and Blood Institute (R01HL093324)
- New York Stem Cell Foundation
- JPB Foundation (P50AG016573)
- Cure Alzheimer's Fund (RF1AG054014, U01AG046170, RF1AG057440, RF1AG074010)
- AbbVie
- Biogen
- Eisai
- National Institutes of Health (RF1AG054014, RF1AG057440, P50AG016573, P30AG066519, RF1AG074010, U01AG046170, K01AG062683, OD 1S10OD010794-01, 1S10OD021718-01)
- University of California, Irvine (P30AG066519)
- GlaxoSmithKline
- National Institute on Aging (U19AG069701, U01AG058635)
- National Institute of Neurological Disorders and Stroke (RF1AG047644, RF1NS090934)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Keywords
- APOE ε4, Alzheimer's disease, astrocytes, microglia, cholesterol metabolism, matrisome, lipid metabolism, de novo cholesterol synthesis, glial activation, chemotaxis, transcriptomics, non-cell-autonomous signaling
- MeSH terms
- Alzheimer Disease, Animals, Apolipoproteins E, Astrocytes, Cholesterol, Humans, Microglia, Mice, Apolipoprotein E3, Apolipoprotein E4, Induced Pluripotent Stem Cells
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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