Evidence map›Paper›PMID 29353455›Full record

ReviewMolecular neurobiology2018

The Interplay Between Apolipoprotein E4 and the Autophagic-Endocytic-Lysosomal Axis.

E Schmukler, D M Michaelson, R Pinkas-Kramarski

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. The connection between autophagy and Alzheimer's disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  5. Interconnections of insulin/IGF-1 signaling and autophagy abnormalities in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  6. Heavy metal-induced disruption of the autophagy-lysosomal pathway: implications for aging and neurodegenerative disorders.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2025
    Review
  7. Genome-wide association analysis identifies APOE as a mitophagy modifier in Lewy body disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  8. Review
  9. Review
  10. Frontiers in aging neuroscience · 2023
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Retinal imaging demonstrates reduced capillary density in clinically unimpairedAlzheimer's & dementia (Amsterdam, Netherlands) · 2021
    Article
  16. Article
  17. Amyloid-beta impairs TOM1-mediated IL-1R1 signaling.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  18. Article
  19. Amyloid clearance defect in ApoE4 astrocytes is reversed by epigenetic correction of endosomal pH.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

E SchmuklerDepartment of Neurobiology, Tel-Aviv University, 69978, Ramat-Aviv, Israel.
D M MichaelsonDepartment of Neurobiology, Tel-Aviv University, 69978, Ramat-Aviv, Israel.
R Pinkas-KramarskiDepartment of Neurobiology, Tel-Aviv University, 69978, Ramat-Aviv, Israel. lironit@post.tau.ac.il.ORCID http://orcid.org/0000-0002-1000-369X
Tel Aviv University · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Since its discovery as a genetic risk factor for Alzheimer's disease, the APOE4 allele has been linked to the majority of the pathological findings associated with the disease progression. These include abnormalities of the endocytic, autophagic, and lysosomal machineries, which begin at the most early stages of Alzheimer's disease development. Considering that these three vesicular systems share common features and, in fact, comprise an interconnected cargo-trafficking and degradation network, some of the effects of APOE4 are interrelated, while others are system-specific. In turn, APOE4-driven impairments of endocytosis, autophagy, and lysosomal activity influence various aspects of Alzheimer's disease pathology, ranging from Aβ generation and clearance to neuronal loss and cognitive deficits. This review discusses the detrimental effects of APOE4 on the endocytic-autophagic-lysosomal axis in the context of Alzheimer's disease, as well as the various mechanisms underlying them.

Indexed as

AutophagyEndocytosisAlzheimer DiseaseAnimalsApolipoprotein E4HumansLysosomesModels, BiologicalApolipoprotein E4Alzheimer’s disease (AD)Amyloid βApolipoprotein E4 (apoE4)AutophagyEndocytosisLysosomal degradation

Identifiers

PMID29353455
OpenAlexW2785279364

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.