Evidence map›Paper›PMID 28085665›Full record

ArticleeLife2017

Impaired retrograde transport of axonal autophagosomes contributes to autophagic stress in Alzheimer's disease neurons.

Prasad Tammineni, Xuan Ye, Tuancheng Feng, Daniyal Aikal, Qian Cai

Open access · goldAbstract read
In one paragraph

Article in eLife, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed
9.7field-weighted citation impact, top 1% 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

109 citing papers in PubMed, 173 citations in OpenAlex.

  1. Article
  2. Article
  3. Dysregulation of autophagosome-mitochondria contacts contributes to autophagy dysfunction and neurodegeneration in tauopathy.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. The impact of ERCell death & disease · 2025
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. Article

49 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 2 countries.

Prasad TammineniDepartment of Cell Biology and Neuroscience, Rutgers, The State University of New Jersey, Piscataway, United States.
Xuan YeDepartment of Cell Biology and Neuroscience, Rutgers, The State University of New Jersey, Piscataway, United States.
Tuancheng FengDepartment of Cell Biology and Neuroscience, Rutgers, The State University of New Jersey, Piscataway, United States.
Daniyal AikalDepartment of Cell Biology and Neuroscience, Rutgers, The State University of New Jersey, Piscataway, United States.
Qian CaiDepartment of Cell Biology and Neuroscience, Rutgers, The State University of New Jersey, Piscataway, United States.ORCID 0000-0001-8525-2749
Rutgers, The State University of New Jersey · US

Funding

The Role of Abnormal Inter-Organelle Communication in the Pathogenesis of TauopathyR01NS089737 · NINDS · RUTGERS, THE STATE UNIV OF N.J. · PI Qian Cai · 2014 to 2026
$5.5M
ROLE OF SNAPIN-MEDIATED LYSOSOMAL REGULATION IN ALZHEIMER'S DISEASE PATHOGENESISR00AG033658 · NIA · RUTGERS, THE STATE UNIV OF N.J. · PI CAI, QIAN · 2012 to 2014
$728k
NIA NIH HHS R00 AG033658NINDS NIH HHS R01 NS089737
6 · The paper itself

Abstract

Neurons face unique challenges of transporting nascent autophagic vacuoles (AVs) from distal axons toward the soma, where mature lysosomes are mainly located. Autophagy defects have been linked to Alzheimer's disease (AD). However, the mechanisms underlying altered autophagy remain unknown. Here, we demonstrate that defective retrograde transport contributes to autophagic stress in AD axons. Amphisomes predominantly accumulate at axonal terminals of mutant hAPP mice and AD patient brains. Amyloid-β (Aβ) oligomers associate with AVs in AD axons and interact with dynein motors. This interaction impairs dynein recruitment to amphisomes through competitive interruption of dynein-Snapin motor-adaptor coupling, thus immobilizing them in distal axons. Consistently, deletion of

Indexed as

AutophagyAlzheimer DiseaseAnimalsAutophagosomesAxonsBiological TransportDyneinsHumansMiceVesicular Transport ProteinsDyneinsSnapin protein, mouseVesicular Transport Proteinsalzheimer'samphisomeautophagic stresscell biologydynein motorhumanmouseneuroscienceretrograde transportSnapin

Identifiers

PMID28085665
PMCPMC5235353
OpenAlexW2577326796

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.