Evidence map›Paper›PMID 33910020›Full record

ArticleCell reports2021

Post-Golgi carriers, not lysosomes, confer lysosomal properties to pre-degradative organelles in normal and dystrophic axons.

Pearl P Y Lie, Dun-Sheng Yang, Philip Stavrides, Chris N Goulbourne, Ping Zheng, Panaiyur S Mohan, Anne M Cataldo, Ralph A Nixon

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
10.1field-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

54 citing papers in PubMed, 91 citations in OpenAlex.

  1. Review
  2. Structural Mechanisms of DNAJC13 Dimeric Assembly and InsPbioRxiv : the preprint server for biology · 2026
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  16. Lysosomes' fallback strategies: more than just survival or death.Frontiers in cell and developmental biology · 2025
    Review
  17. Review
  18. Article
  19. Review
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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

8 authors at 3 institutions in 1 country.

Pearl P Y LieCenter for Dementia Research, Nathan S. Kline Institute, Orangeburg, NY 10962, USA; Department of Psychiatry, New York University Langone Medical Center, New York, NY 10016, USA.
Dun-Sheng YangCenter for Dementia Research, Nathan S. Kline Institute, Orangeburg, NY 10962, USA; Department of Psychiatry, New York University Langone Medical Center, New York, NY 10016, USA.
Philip StavridesCenter for Dementia Research, Nathan S. Kline Institute, Orangeburg, NY 10962, USA.
Chris N GoulbourneCenter for Dementia Research, Nathan S. Kline Institute, Orangeburg, NY 10962, USA.
Ping ZhengCenter for Dementia Research, Nathan S. Kline Institute, Orangeburg, NY 10962, USA.
Panaiyur S MohanCenter for Dementia Research, Nathan S. Kline Institute, Orangeburg, NY 10962, USA; Department of Psychiatry, New York University Langone Medical Center, New York, NY 10016, USA.
Anne M CataldoMcLean Hospital, Harvard Medical School, Belmont, MA 02478, USA.
Ralph A NixonCenter for Dementia Research, Nathan S. Kline Institute, Orangeburg, NY 10962, USA; Department of Psychiatry, New York University Langone Medical Center, New York, NY 10016, USA; Department of Cell Biology, New York University Langone Medical Center, New York, NY 10016, USA; NYU Neuroscience Institute, New York University Langone Medical Center, New York, NY 10016, USA. Electronic address: nixon@nki.rfmh.org.
Nathan Kline Institute for Psychiatric Research · USNYU Langone Health · USMcLean Hospital · US

Funding

Uncovering Alzheimer's disease risk mechanisms through neuron-specific analysis of autophagy and endosomal-lysosomal functionP01AG017617 · NIA · NATHAN S. KLINE INSTITUTE FOR PSYCH RES · PI NIXON, RALPH A. · 2000 to 2021
$40.0M
Endosome Dysfunction in Alzheimer's DiseaseR01AG062376 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI NIXON, RALPH A. · 2018 to 2022
$3.7M
NIA NIH HHS P01 AG017617NIA NIH HHS R01 AG062376
6 · The paper itself

Abstract

Lysosomal trafficking and maturation in neurons remain poorly understood and are unstudied in vivo despite high disease relevance. We generated neuron-specific transgenic mice to track vesicular CTSD acquisition, acidification, and traffic within the autophagic-lysosomal pathway in vivo, revealing that mature lysosomes are restricted from axons. Moreover, TGN-derived transport carriers (TCs), not lysosomes, supply lysosomal components to axonal organelles. Ultrastructurally distinctive TCs containing TGN and lysosomal markers enter axons, engaging autophagic vacuoles and late endosomes. This process is markedly upregulated in dystrophic axons of Alzheimer models. In cultured neurons, most axonal LAMP1 vesicles are weakly acidic TCs that shuttle lysosomal components bidirectionally, conferring limited degradative capability to retrograde organelles before they mature fully to lysosomes within perikarya. The minor LAMP1 subpopulation attaining robust acidification are retrograde Rab7

Indexed as

AnimalsAxonsDisease Models, AnimalGolgi ApparatusMiceMice, TransgenicOrganellesacidificationautophagic vacuoleaxonal transportLAMP1late endosomelysosomepost-Golgi traffictransport carrier

Identifiers

PMID33910020
PMCPMC8135226
OpenAlexW3158880539

What OpenQuestion holds

Textmetadata
LicenceTDM
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.