Evidence map›Paper›PMID 29626653›Full record

ReviewNeuroscience letters2019

Neuronal lysosomes.

Shawn M Ferguson

Abstract readReview
In one paragraph

Review in Neuroscience letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

60 citing papers in PubMed, 100 citations in OpenAlex.

  1. Late Endosome Transport by RILP-RAB7A Promotes Dendrite Arborization Independently of Degradation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Article
  2. Review
  3. Metabolic trajectories in developing human neocortical neurons.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Late endosome transport by RILP-RAB7A promotes dendrite arborization.bioRxiv : the preprint server for biology · 2025
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Huntingtin contains an ubiquitin-binding domain and regulates lysosomal targeting of mitochondrial and RNA-binding proteins.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  19. Article
  20. Article
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

1 author at 1 institution in 1 country.

Shawn M FergusonDepartment of Cell Biology, Yale University School of Medicine, New Haven, CT, 06510, United States; Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT, 06510, United States. Electronic address: shawn.ferguson@yale.edu.
Yale University · US

Funding

Yale Alzheimer Disease Research CenterP50AG047270 · NIA · YALE UNIVERSITY · PI KWAN, CHUN-HAY ALEX · 2015 to 2019
$8.3M
Molecular mechanisms that match lysosome function to cellular demandR01GM105718 · NIGMS · YALE UNIVERSITY · PI FERGUSON, SHAWN · 2013 to 2022
$2.9M
NIA NIH HHS P50 AG047270NIGMS NIH HHS R01 GM105718
6 · The paper itself

Abstract

Lysosomes support diverse cellular functions by acting as sites of macromolecule degradation and nutrient recycling. The degradative abilities of lysosomes are conferred by a lumen that is characterized by an acidic pH and which contains numerous hydrolases that support the breakdown of major cellular macromolecules to yield cellular building blocks (amino acids, nucleic acids, sugars, lipids and metals) that are transported into the cytoplasm for their re-use. In addition to these important hydrolytic and recycling functions, lysosomes also serve as a signaling platform that integrates nutrient and metabolic cues to control signaling via the mTORC1 pathway. Due to their extreme longevity, polarity, demands of neurotransmission and metabolic activity, neurons are particularly sensitive to perturbations in lysosome function. The dependence of neurons on optimal lysosome function is highlighted by insights from human genetics that link lysosome dysfunction to a wide range of both rare and common neurological diseases. How then is lysosome function adapted to the unique demands of neurons? This review will focus on the roles played by lysosomes in distinct neuronal sub-compartments, the regulation of neuronal lysosome sub-cellular localization and the implications of such neuronal lysosome regulation for both physiology and disease.

Indexed as

AnimalsAutophagyHumansLysosomesNeuronsAlzheimer's diseaseAutophagosomeAxonDendriteEndosomeHereditary spastic paraplegiaLysosomemTORC1

Identifiers

PMID29626653
PMCPMC6170731
OpenAlexW4210958114

What Socratic 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 Socratic graph.