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PreprintCited by 0Alzheimer's disease research and treatmentsLipid metabolism and biosynthesisAutophagy in Disease and Therapy

The DOI matches its Crossref record; 88 of the 89 references it cites were found in a registry or an index; 16 of the 27 sources its claims cite were checked for support.

ApoE4 impairs astrocyte lipid droplet formation via endolysosomal dysfunction

Open access
Ralhan, Isha, Bae, Ju-Young, Lee, Nathanael YJ, Cai, Wendy, Chang, Jinlan, Jarad, Suha, Gu, Hongmei, Zhang, Dawei, Ioannou, Maria S.·2026·bioRxiv (Cold Spring Harbor Laboratory)
DOI 10.64898/2026.09.01.748585
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Abstract

SUMMARY: An important component of neuron-glia coupling is the transport and delivery of neuron-derived lipids to glial lipid droplets. This pathway is important as failure to store incoming lipids in glial lipid droplets exacerbates neurodegeneration. ApoE4, a risk factor for Alzheimer’s disease, impairs this transport pathway. But how ApoE4 affects lipid trafficking in glia and whether these alterations can be restored is poorly understood. Here, we demonstrate that ApoE4 particles impair endolysosomal function and promote lipofuscin formation in cultured primary astrocytes, thereby disrupting the trafficking of lipids for storage into lipid droplets. Lipid droplets, however, can be recovered by preventing lysosomal impairment with PCSK9, a secreted protein that prevents LDLR recycling and reduces ApoE4 internalization. Lipid droplets are similarly recovered in the presence of ApoE4 by repairing endolysosomal function. Our findings reveal new insight into how ApoE4 dysregulates lipid storage while uncovering new mechanisms to correct these defects. Graphical Abstract:

Overview

AI snapshot

Written from the paper’s full text.

TL;DR

ApoE4 particles impair endolysosomal function and promote lipofuscin formation in cultured primary astrocytes, reducing the trafficking and storage of neuron-derived lipids into lipid droplets. Preventing ApoE4 internalization with PCSK9 or restoring endolysosomal function with rimeporide or YM-201636 recovers lipid droplet formation.

Key findings

  • ApoE genotype influenced neuron-to-astrocyte fatty acid transfer: ApoE2 astrocytes had the highest neuron-derived Red-C12, while ApoE4 astrocytes had the least, regardless of neuronal genotype. Exogenous ApoE2 particles enhanced Red-C12 transfer, whereas ApoE4 particles failed to increase it and decreased Red-C12 puncta in ApoE3 astrocytes; Aβ42 reduced transfer, and ApoE2 but not ApoE4 particles continued to enhance it.
  • ApoE4 particles decreased the number and size of BD493-positive lipid droplets and reduced triglycerides in wild-type astrocytes, but did not affect lipid droplets in ApoE4 astrocytes. Approximately 76% of BD493 puncta colocalized with the lipid droplet marker mApple-6xHp.
  • ApoE4 particles decreased LysoTracker-positive puncta and cathepsin D activity, and increased autofluorescent lipofuscin-like puncta. Roughly 30% of lipofuscin-like autofluorescence colocalized with Rab7, about 35% of ApoE4 puncta colocalized with Rab7, and 30% of ApoE4 puncta were positive for GFP-LC3.
  • PCSK9 reduced ApoE4 particle internalization and prevented ApoE4-mediated lipofuscin accumulation and lipid droplet reduction. Rimeporide or YM-201636 rescued LysoTracker-positive puncta, cathepsin D activity, lipofuscin formation, lipid droplet number/size, and triglyceride levels in the presence of ApoE4 particles.

Methods

  • Primary hippocampal neurons and astrocytes were cultured from wild-type Sprague Dawley rats or targeted replacement rats expressing human ApoE2, ApoE3, or ApoE4; glial cultures were >95% GFAP-positive and neuronal cultures 97% β3-tubulin-positive.
  • Fatty acid transfer assays used neurons loaded with BODIPY 558/568 C12 (Red-C12) and unlabelled astrocytes on separate coverslips separated by paraffin wax in HBSS, with ApoE particles (POPC plus human ApoE2/E3/E4, approximately 10–20 nm by TEM) at 50 µg/ml, with or without 2 µM Aβ42. Lipid droplets, LysoTracker, lipofuscin autofluorescence, ApoE colocalization, cathepsin D activity, triglycerides, and ApoE internalization by western blot were assessed after treatments including PCSK9 (10 µg/ml), bafilomycin A1, rimeporide (10 µM), and YM-201636 (200 nM).
  • Imaging used Airyscan confocal microscopy and Fiji-ImageJ quantification; statistical analyses used GraphPad Prism with one-way ANOVA/Tukey, two-tailed Student’s t tests, or one-sample t tests with Bonferroni correction where stated, based on independent replicates.

Limitations

  • The paper states that it was unable to detect isoform-dependent differences in ApoE uptake by astrocytes, and notes that the assay may not be sensitive enough to detect subtle differences.
  • The paper states that PCSK9 effects may not be specific to LDLR because PCSK9 can also target VLDLR, ApoER2, and LRP1; it also cautions that PIKfyve inhibition may have unfavourable effects on autophagy and lysosomal function, and that NHE-1 targeting is not specific to endolysosomes.
  • The paper notes that acute treatment likely captured late endosomes in early stages of lipofuscin formation and that it remains unclear at what stage lipofuscin becomes indigestible. Evident from the text: the study is in primary rat cultures under starvation/HBSS conditions, focuses largely on wild-type astrocytes after initial genotype comparisons, and does not report in vivo or neurodegeneration outcomes.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.64898/2026.09.01.748585

Cites

88 of 89 references verified1 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Verification

Claims the paper makes

16 of 27 cited sources checked · 5 supported · 2 flagged · accuracy not yet measured

  • Premisecitation

    ApoE4 is less efficient at being internalized by astrocytes through LDLR.

    “ApoE4 is also less efficient at being internalized by astrocytes through LDLR 14 .”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [14] source

      The Results section (“LipApoE3/E4 alter cellular distribution of LDLR and impair LDL uptake”) reports greater internalized lipidated ApoE4 than ApoE3 or ApoE2 in iPSC-derived astrocytes, rather than less efficient ApoE4 internalization. The Results section (“Cellular uptake of ApoE by LDLR is isoform-dependent”) also says that blocking LDLR inhibited ApoE3/E4 uptake in those astrocytes. Page numbers were not provided in our copy. (LLM, conf=0.90)

      Checked by a reasoning model — may be wrong.

      Experimental — accuracy not yet measured
  • Premisecitation

    Astrocytes expressing ApoE4 typically have more lipid droplets compared to those expressing ApoE2 or ApoE3.

    “Astrocytes expressing ApoE4 typically have more lipid droplets compared to those expressing ApoE2 or ApoE3 [49][50][51][52][53] .”
    Quote in the paperSubstantial claim4 of 5 sources checked
    • cites [49] source

      The Results section, “Human iPSC-derived APOE4-expressing astrocytes display intracellular lipid dysregulation” (page unavailable), reports more lipid droplets in APOE4 than APOE3 astrocytes across two pairs of isogenic iPSC-derived lines. It does not report a lipid-droplet comparison with APOE2 astrocytes, so that part of the claim is unsupported by this paper. (LLM, conf=0.89)

      Experimental — accuracy not yet measured
    • cites [50] source

      The Results section, “APOE4 expression results in large LDs with impaired turnover” (page unavailable), reports no difference in droplet number between APOE4 and APOE3 astrocytes at baseline or after pulse-chase, and fewer droplets in APOE4 cells after an oleic-acid pulse. The cited paper does not provide an APOE2 comparison in these passages. It therefore does not support the claim that APOE4 astrocytes typically have more droplets. (LLM, conf=0.90)

      Checked by a reasoning model — may be wrong.

      Experimental — accuracy not yet measured
    • cites [51] source

      The paper’s introductory passage reports greater lipid-droplet accumulation in APOE4-expressing astrocytes than in APOE3-expressing astrocytes, but does not make that comparison with APOE2. In “Augmentation of cholesterol esterification and lipid droplet accumulation by 25HC” (page unavailable), its own experiment found no obvious APOE3–APOE4 difference at the 25HC concentrations tested. (LLM, conf=0.88)

      Experimental — accuracy not yet measured
    • cites [52] source

      Results §3.1 reports significantly more lipid droplets in E4 than E3 astrocytes, both at baseline and after fatty-acid loading. The reported comparison is with E3; the paper does not establish the claimed comparison with E2. (LLM, conf=0.90)

      Experimental — accuracy not yet measured
    • cites [53] source
  • Premisecitation

    Lysosomal degradation is an important source of lipids to be stored in lipid droplets.

    “Lysosomal degradation is an important source of lipids to be stored in lipid droplets 12,27 .”
    Quote in the paperSubstantial claim2 of 2 sources checked
  • Premisecitation

    LDLR is a key receptor for ApoE-mediated uptake by astrocytes.

    “LDLR is a key receptor for ApoEmediated uptake by astrocytes 13,14 .”
    Quote in the paperSubstantial claim2 of 2 sources checked
    • cites [13] source

      The Results and Figure 1 report that LDLR mediates uptake of astrocyte-secreted apoE-containing particles. The uptake experiments used mouse embryonic fibroblasts and Chinese hamster ovary cells, however, not astrocytes; the paper does not establish uptake by astrocytes themselves. Page numbers are unavailable in our copy. (LLM, conf=0.88)

      Experimental — accuracy not yet measured
    • cites [14] source
  • Premisecitation

    Starvation-induced lipid droplets are prevented by inhibiting lysosomal acidification and degradative function with bafilomycin A1.

    “Previous work found that starvation-induced lipid droplets are prevented by inhibiting lysosomal acidification and degradative function with bafilomycin A1 12,34 .”
    Quote in the paperSubstantial claim1 of 2 sources checked
    • cites [12] source
    • cites [34] source

      Checked before — its earlier verdict is held back until a new check runs.

  • It may state two separate claims as one. 14
  • Probably not a substantial claim. 15

  • It may state two separate claims as one.

    Premisecitation

    PCSK9 prevents LDLR recycling and reduces ApoE uptake.

    “The activity of LDLR is tightly regulated by PCSK9, as it prevents its recycling to the surface and subsequently reduces ApoE uptake [31][32][33] .”
    Quote in the paperSubstantial claim1 of 3 sources checked
    • cites [31] source

      The Discussion (page not specified in our copy) says PCSK9 binding is consistent with a model in which LDLR fails to recycle to the cell surface and is degraded. It identifies apolipoprotein E as an LDLR ligand, but does not report reduced ApoE uptake; the Discussion says the effect of PCSK9 binding on lipoprotein binding remains to be determined. (LLM, conf=0.87)

      Experimental — accuracy not yet measured
    • cites [32] Zhang, D.-W. , Garuti, R. , Tang, W.-J. , Cohen, J.C. , and Hobbs, H.H. (2008). Structural requirements for PCSK9-mediated degradation of the low-density lipoprotein receptor. source

      Checked before — its earlier verdict is held back until a new check runs.

    • cites [33] source

      Checked before — its earlier verdict is held back until a new check runs.

  • It may state two separate claims as one.

    Premisecitation

    Endolysosomal dysfunction is prominent in glia expressing ApoE4 as well as in neurons treated with ApoE4 particles.

    “Endolysosomal dysfunction is also prominent in glia expressing ApoE4 as well as in neurons treated with ApoE4 particles 10,14,15 .”
    Quote in the paperSubstantial claim2 of 3 sources checked
    • cites [10] source
    • cites [14] source

      The Results section reports that ApoE4 particles carrying CE(20:4) induced lipofuscin accumulation in treated human iPSC-derived neurons, supporting the neuronal part of the claim. In APOE4 knock-in mice, however, the Results describe lipofuscin as predominantly neuronal and only occasionally detected in microglia; the paper does not establish prominent endolysosomal dysfunction across glia expressing ApoE4. Page numbers are not available in our copy. (LLM, conf=0.86)

      Experimental — accuracy not yet measured
    • cites [15] source

      The Discussion reports APOE4-associated endosomal–lysosomal dysregulation in aged mouse brains, and the Results identify abnormalities in neurons. The paper does not establish dysfunction specifically in glia expressing APOE4 or in neurons treated with APOE4 particles; its measurements were made in APOE4-expressing mice. (LLM, conf=0.86)

      Experimental — accuracy not yet measured

  • It may state two separate claims as one.

    Findingown data

    ApoE4 particles decrease the number of LysoTracker-positive puncta, while ApoE2 and ApoE3 particles have no effect.

    “We found that ApoE4 particles decreased the number of LysoTracker-positive puncta, while ApoE2 and ApoE3 particles had no effect (Figures 3A and 3B).”
    Quote in the paperSubstantial claim

  • It may state two separate claims as one.

    Findingown data

    Bafilomycin A1 reduced the number of LysoTracker-positive puncta and the number and size of lipid droplets in astrocytes.

    “We confirmed that bafilomycin A1 similarly reduced the number of LysoTracker-positive puncta (Figures S4A-S4C) and the number and size of lipid droplets in astrocytes (Figures S4D-S4F).”
    Quote in the paperSubstantial claim

  • It may state two separate claims as one.

    Findingown data

    In the presence of Aβ42, ApoE2 particles continue to enhance Red-C12 transport while ApoE4 particles are unable to do so.

    “ApoE2 particles continued to enhance Red-C12 transport in the presence of Aβ42, while ApoE4 120 particles were unable to do so (Figures 1J, 1K, S1H, and S1I).”
    Quote in the paperSubstantial claim

  • It may state two separate claims as one.

    Findingown data

    Extracellular ApoE4 particles fail to increase neuron-derived Red-C12 detected in astrocytes, whereas ApoE2 particles enhance it.

    “Addition of ApoE2 particles enhanced the amount 110 of neuron-derived Red-C12 detected in ApoE3 and ApoE4 astrocytes (Figures 1D-1G).ApoE4 particles, on the other hand, failed to increase neuron-derived Red-C12 detected in astrocytes (Figures 1D-1G).”
    Quote in the paperSubstantial claim

  • It may state two separate claims as one.

    Findingown data

    ApoE4 co-localization with Rab7-positive late endosomes is increased compared to ApoE2, accounting for roughly 35% of ApoE4 puncta.

    “We observed an increase in ApoE4 co-195 localization with Rab7-positive late endosomes as compared to ApoE2, accounting for roughly 35% of the ApoE4 puncta (Figures 3I and 3J).”
    Quote in the paperSubstantial claim

  • It may state two separate claims as one.

    Findingown data

    In ApoE4-treated astrocytes, lipofuscin-like material is present in electron-lucent endosomes and electron-dense compartments.

    “Arrows highlight lipofuscin-like material in electron-lucent endosomes.Arrowhead highlights lipofuscin-like material in electrondense compartments.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.

    Findingown data

    ApoE particles are approximately 10-20 nm in diameter, with ApoE4 showing a slight but nonsignificant reduction in size compared to other isoforms.

    “The ApoE particles were approximately 10-20 nm in diameter as confirmed by transmission electron microscopy, with ApoE4 particles showing a slight but nonsignificant reduction in size compared to the other isoforms 20 (Figures S1F and S1G).”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Findingown data

    No significant differences in ApoE particle diameter were discovered among ApoE2, ApoE3, and ApoE4 particles.

    “Size distribution of ApoE particle diameters determined by TEM.n = 3 technical replicates; mean ± SD.One-way ANOVA with Tukey's post-test.ns, no significant differences were discovered.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Findingown data

    In ApoE4 astrocytes, there are no ApoE-isoform specific differences on lipid storage.

    “Figure S2. No ApoE-isoform specific differences on lipid storage in ApoE4 astrocytes”
    • Also stated in: § 745 · plain
      “ns, no significant differences were discovered.”
    Quote in the paperNot a substantial claim

  • It may state two separate claims as one.

    Interpretationown data

    ApoE4 particles impair endolysosomal function and promote lipofuscin formation in cultured primary astrocytes, thereby disrupting the trafficking of lipids for storage into lipid droplets.

    “Here, we demonstrate that ApoE4 particles impair endolysosomal function and promote lipofuscin formation in cultured primary astrocytes, thereby disrupting the trafficking of lipids for storage into lipid droplets.”
    • Also stated in: § DISCUSSION 265 · plain
      “We show that uptake of ApoE4 on lipoprotein-like particles impairs endolysosomal function.This prevents the degradation of lipids resulting in lipofuscin formation and limits the supply of lipids for storage in lipid droplets.”
    Quote in the paperSubstantial claim

  • It may state two separate claims as one.

    Interpretationreasoning

    Under starvation conditions, ApoE4 reduced the formation of lipid droplets, opposite to nutrient-rich conditions where ApoE4 astrocytes typically have more lipid droplets.

    “Under these conditions, as opposed to increased lipid droplets, we find the opposite to be true, that ApoE4 reduced the formation of lipid droplets.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Premisecitation

    PCSK9 dampens the uptake of ApoE lipoprotein particles.

    “In 65 doing so, PCSK9 dampens the uptake of ApoE lipoprotein particles.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [16] source

      Checked before — its earlier verdict is held back until a new check runs.

  • It may state two separate claims as one.

    Interpretationown data

    Lipid droplets can be recovered by preventing lysosomal impairment with PCSK9, which prevents LDLR recycling and reduces ApoE4 internalization.

    “Lipid droplets, however, can be recovered by preventing lysosomal impairment with PCSK9, a secreted protein that prevents 25 LDLR recycling and reduces ApoE4 internalization.”
    • Also stated in: § PCSK9 prevents ApoE4-mediated lipofuscin formation and drop in lipid storage · hedged
      “These results suggest that astrocytic lipid droplets are influenced by the uptake of ApoE and this can be regulated by PCSK9.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Premisecitation

    Lipofuscin is characterized by the accumulation of undigested material including oxidized lipids within non-degradative lysosomes.

    “Lipofuscin is characterized by the accumulation of undigested material including oxidized lipids within non-degradative lysosomes 28 .”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [28] source

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Study design and conductnone given

    The PCSK9 and YM-201636 lipid droplet assays were quantified blind.

    “The PCSK9 and YM-201636 lipid droplet assays were quantified blind.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Study design and conductnone given

    The imaging field of view was selected using the DAPI channel to blind the experimenter to the β3-tubulin, GFAP and Iba1 channels.

    “The imaging field of view was selected using the DAPI 470 channel to blind the experimenter to the β3-tubulin, GFAP and Iba1 channels.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.

    Premisecitation

    ApoE4 carrying polyunsaturated cholesterol esters induced lysosomal defects and lipofuscin accumulation.

    “This supports recent work demonstrating that ApoE4 320 carrying polyunsaturated cholesterol esters induced lysosomal defects and lipofuscin accumulation 14 .”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [14] source

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Study design and conductnone given

    The imaging field of view was selected using the DAPI channel to blind the experimenter to the LysoTracker Red channel.

    “The imaging field of view was selected 590 using the DAPI channel to blind the experimenter to the LysoTracker Red channel.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Study design and conductnone given

    The imaging field of view was selected using the DAPI channel to blind the experimenter to the Red-C12 channel.

    “The imaging field of view was selected using the DAPI channel to blind the experimenter to the Red-C12 channel.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Study design and conductnone given

    The ApoE particle reduced serum lipid droplet assays were imaged and quantified blind.

    “The ApoE particle reduced serum lipid droplet assays were imaged and quantified blind.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Study design and conductnone given

    The imaging field of view was selected using the DAPI channel to blind the experimenter to the autofluorescent channel.

    “The imaging field of view was selected using the DAPI channel to blind the experimenter to the autofluorescent channel.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Study design and conductnone given

    The imaging field of view was selected using the DAPI channel to blind the experimenter to the other channels in lipid droplet assays.

    “The imaging field of view was selected using the DAPI channel to blind the experimenter to the other channels.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Study design and conductown data

    97% of neuronal cultures stained positive for β3-tubulin.

    “While 97% percent of neuronal cultures stained positive for the neuron-specific β3-tubulin (Figures S1D and S1E).”
    Quote in the paperNot a substantial claim

  • It may state two separate claims as one.

    Premisecitation

    ApoE4 particles extract less unsaturated phospholipids from neurons, but no difference in saturated Red-C12 efflux was observed.

    “Indeed, we previously found that ApoE4 particles extract less unsaturated phospholipids from neurons, however no difference in the 130 amount of saturated Red-C12 efflux was observed 10 .”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [10] source

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Study design and conductnone given

    For all co-localization assays, the imaging field of view was selected using the DAPI channel to blind the experimenter to the other channels.

    “For all co-localization assays, the imaging field of view was selected using the DAPI channel to blind the experimenter to the other channels.”
    Quote in the paperNot a substantial claim
27 of 27

  • The paper relies on this without support.

    The ApoE particles composed of 16:0-18:1 phosphatidylcholine and human ApoE2/3/4 adequately mimic native ApoE lipoproteins in the brain.

    “To explore this, we 105 repeated the Red-C12 transfer assay in the presence of exogenous particles composed of 16:0-18:1 phosphatidylcholine and human ApoE2, ApoE3 or ApoE4 10 (Figures S1F and S1G).”

  • The paper relies on this without support.

    Lipofuscin-like autofluorescence is a valid proxy for oxidized lipid accumulation.

    “Here, we assessed lipofuscin-like autofluorescence as a proxy for oxidized lipid accumulation that could be resolved when lysosomal function was improved.”
2 of 2

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • GFP-LC3 co-localization uses conflicting denominators

    Major

    The Results describe the percentage as a fraction of ApoE4 puncta, but the Methods define it as a fraction of GFP-LC3 puncta. These are different measures, so the stated 30% cannot be interpreted unambiguously.

  • Cathepsin D figure legend names neurons as the control

    Minor

    The figure legend says cathepsin D activity was normalized to control neurons, whereas the corresponding assay in the Methods uses astrocytes and describes normalization to a control treatment.

  • Red-C12 release figure legend names neurons as the control

    Minor

    Figure 2A says the astrocyte-conditioned-medium signal was normalized to control neurons, but the described release assay loads and collects medium from astrocytes.

3 of 3

Cited works that were retracted

Works this paper cites that were later retracted, from the retraction notices publishers deposit. Major when the notice came out before this paper was published.

  • Cites a retracted work: 10.1016/j.celrep.2025.116179

    Major

    The cited work was retracted on 2025-09-23 (notice 10.1016/j.celrep.2025.116179), before this paper was published (2026-09-04). Its authors could have known.

    Cited work 10.1016/j.celrep.2025.116179 · retracted 2025-09-23 · notice 10.1016/j.celrep.2025.116179 · this paper published 2026-09-04

1 of 1

Citations

Cites

1 retracted

Flagged first, then by citations

Research works printed but not linked: 1

  1. 10.1016/j.cell.2019.1004.1001 · DOI

Cited by

Still being checked.

Related

Metadata

Authors
Ralhan, I., Bae, J.-Y., Lee, N. Y., Cai, W., Chang, J., Jarad, S., Gu, H., Zhang, D., & Ioannou, M. S.
Affiliations
University of Alberta (CA)
Corresponding author
Ioannou, Maria S.
ORCID
Venue
bioRxiv (Cold Spring Harbor Laboratory)
Publisher
openRxiv
Published
2026-09-04
DOI
10.64898/2026.09.01.748585
OpenAlex
W7208835235
Semantic Scholar
992d8e7f5208905c8607dffe7a6df1eedde93d3e
Cited by
0
References
80
Type
posted content
Language
en
Open access
Licence
Locations
bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion, cc-by-nc-nd)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
Keywords
APOE ε4, astrocytes, lipid droplets, endolysosomal dysfunction, lipofuscin, lipid trafficking, PCSK9, Alzheimer's disease, neurodegeneration

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