Evidence map›Paper›PMID 29859318›Full record

ReviewNeurobiology of disease2019

Lysosome trafficking and signaling in health and neurodegenerative diseases.

Pearl P Y Lie, Ralph A Nixon

Open access · greenAbstract readReview
In one paragraph

Review in Neurobiology of disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 166 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
166citing papers in PubMed, 2 pooled it
23.2field-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

166 citing papers in PubMed, 2 syntheses or guidelines pooled it, 257 citations in OpenAlex.

  1. Pooled it
  2. Guideline
  3. Article
  4. Review
  5. Microglia extract neuronal proteolytic organelles via skoupocytosis.bioRxiv : the preprint server for biology · 2026
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Lysosomal homeostasis at the crossroads of neurodegeneration.The Journal of clinical investigation · 2026
    Review
  13. Article
  14. Article
  15. Enhanced lysosomal activity prevents infection with PrPThe Journal of biological chemistry · 2026
    Article
  16. Article
  17. Article
  18. Article
  19. Autophagy-lysosomal pathway in neurodegeneration.Molecular neurodegeneration advances · 2026
    Review
  20. Review

106 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

2 authors at 2 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. Electronic address: plie@nki.rfmh.org.
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.
Nathan Kline Institute for Psychiatric Research · USNYU Langone Health · 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
DYNAMICS OF THE NEURONAL CYTOSKELETON IN AGING BRAINR01AG005604 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI NIXON, RALPH A. · 1985 to 2014
$4.5M
NIA NIH HHS P01 AG017617NIA NIH HHS R01 AG005604
6 · The paper itself

Abstract

Lysosomes, single-membrane organelles defined by a uniquely strong acidic lumenal pH and high content of acid hydrolases, are the shared degradative compartments of the endocytic and autophagic pathways. These pathways, and especially lysosomes, are points of particular vulnerability in many neurodegenerative diseases. Beyond the role of lysosomes in substrate degradation, new findings have ascribed to lysosomes the leading role in sensing and responding to cellular nutrients, growth factors and cellular stress. This review aims to integrate recent concepts of basic lysosome biology and pathobiology as a basis for understanding neurodegenerative disease pathogenesis. Here, we discuss the newly recognized signaling functions of lysosomes and specific aspects of lysosome biology in neurons while re-visiting the classical defining criteria for lysosomes and the importance of preserving strict definitions. Our discussion emphasizes dynein-mediated axonal transport of maturing degradative organelles, with further consideration of their roles in synaptic function. We finally examine how distinctive underlying disturbances of lysosomes in various neurodegenerative diseases result in unique patterns of auto/endolysosomal mistrafficking. The rapidly emerging understanding of lysosomal trafficking and disruptions in lysosome signaling is providing valuable clues to new targets for disease-modifying therapies.

Indexed as

AnimalsHumansLysosomesNeurodegenerative DiseasesNeuronsAutophagyAxonal transportDyneinLysosomal signalingLysosomeLysosome positioningNeurodegenerative diseaseNutrient-sensing

Identifiers

PMID29859318
PMCPMC6381838
OpenAlexW2806809913

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.