Evidence map›Paper›PMID 30936119›Full record

ReviewCold Spring Harbor perspectives in biology2020

The Autophagy Lysosomal Pathway and Neurodegeneration.

Steven Finkbeiner

Abstract readReview
In one paragraph

Review in Cold Spring Harbor perspectives in biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

100 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Autophagy-lysosomal pathway in neurodegeneration.Molecular neurodegeneration advances · 2026
    Review
  13. Article
  14. Article
  15. Article
  16. Digital neuropathology of neurodegenerative disorders: Foundations, research advances, and future directions.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  17. Article
  18. Article
  19. Review
  20. Review

40 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

1 author.

Steven FinkbeinerGladstone Institutes, San Francisco, California 94158.

Funding

The proteasome in aging and neurodegenerative diseaseP01AG054407 · NIA · NORTHWESTERN UNIVERSITY · PI FINLEY, DANIEL J · 2018 to 2022
$14.0M
Rare Variant Whole Genome Analysis and iPSC Validation of Putative Genetic Modifiers of Huntington DiseaseR37NS101996 · NINDS · J. DAVID GLADSTONE INSTITUTES · PI FINKBEINER, STEVEN M · 2017 to 2023
$4.4M
Dysfunction of the Autophagy-Lysosomal Pathway as a Common Mechanism of NeurodegenerationRF1AG058476 · NIA · J. DAVID GLADSTONE INSTITUTES · PI FINKBEINER, STEVEN M · 2017 to 2018
$4.1M
Tauopathy in AD and FTD - Molecular Determinants of Phenotypic DiversityRF1AG056151 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI CARLSON, GEORGE A., DUFF, KAREN · 2017 to 2017
$4.1M
Retromer dysfunction in amyotrophic lateral sclerosisF31NS101966 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI PEREZ-TORRES, EDUARDO JOSE · 2017 to 2019
$111k
NIA NIH HHS P01 AG054407NIA NIH HHS RF1 AG056151NIA NIH HHS RF1 AG058476NINDS NIH HHS F31 NS101966NINDS NIH HHS R37 NS101996
6 · The paper itself

Abstract

The autophagy lysosomal pathway (ALP) is a major mechanism for degrading intracellular macromolecules. The catabolic products can then be used by the cell for energy or as building blocks to make other macromolecules. Since its discovery, a variety of cellular pathways have emerged that target components with varying specificity for lysosomal degradation. Under some circumstances, lysosomes may release their contents into the extracellular space where they may serve signaling or pathogenic functions. The ALP is active in healthy cells, and the level of activity can be regulated by nutrient-sensing and metabolic signaling pathways. The ALP is the primary pathway by which lipids and damaged organelles are degraded and may be the only pathway capable of degrading aggregated proteins. As such, there has been intense interest in understanding the role of the ALP in the accumulation of aggregated misfolded proteins characteristic of many of the major adult-onset neurodegenerative diseases. This review focuses on recent advances in our understanding of the ALP and its potential relationship to the pathogenesis and treatment of neurodegenerative diseases.

Indexed as

AnimalsAutophagyHumansLipidsLysosomesMolecular ChaperonesNeurodegenerative DiseasesParkinson DiseasePinocytosisSignal TransductionLipidsMolecular Chaperones

Identifiers

PMID30936119
PMCPMC6773515

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.