Cited by 196Autophagy in Disease and TherapyAlzheimer's disease research and treatmentsParkinson's Disease Mechanisms and Treatments

The Autophagy Lysosomal Pathway and Neurodegeneration

Open access
Finkbeiner, Steven·2020·Cold Spring Harbor Perspectives in Biology

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.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1101/cshperspect.a033993

Cites

221 of 221 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Molecular and histopathologic analyses of patient tissues demonstrate mislocalized or accumulated autophagy machinery, pathogenic mutations underlying familial neurodegenerative diseases disable known autophagy-related factors, and genetically ablating autophagy effectors produces neurodegeneration in cell and animal model systems, supporting a role for autophagy dysfunction in age-related neurode

    “Molecular and histopathologic analyses of patient tissues demonstrate mislocalized or accumulated autophagy machinery, pathogenic mutations underlying familial neurodegenerative diseases disable known autophagy-related factors, and genetically ablating autophagy effectors produce neurodegeneration in cell and animal model systems [74–81], supporting a role for autophagy dysfunction in the devel”

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

1 retracted

Flagged first, then by citations

1 of the 222 references couldn’t be matched to a known paper.

Cited by

Sorted by citations

Authors
Finkbeiner, S.
Affiliations
Gladstone Institutes (US)
Corresponding author
Finkbeiner, Steven
Venue
Cold Spring Harbor Perspectives in Biology
Published
2019-04-01
Volume
12
Issue
3
Pages
a033993
ISSN
1943-0264 (ISSN-L)
OpenAlex
W2926862397
Cited by
196
References
222
Citations by year
2026: 25 · 2025: 40 · 2024: 25 · 2023: 19 · 2022: 24 · 2021: 47 · 2020: 10 · 2019: 6
Type
posted content
Language
en
Open access
Locations
  • Cold Spring Harbor Perspectives in Biology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • eScholarship (California Digital Library) (submittedVersion)
Funders
  • National Institute on Aging (RF1AG056151, RF1AG058476, P01AG054407)
  • National Institute of Neurological Disorders and Stroke (F31NS101966, R37NS101996)
Topics
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
Keywords
autophagy-lysosome pathway, neurodegeneration, protein aggregation, misfolded proteins, lysosomal degradation, nutrient sensing, metabolic signaling, lipid degradation, organelle degradation, neurodegeneration pathogenesis, neurodegenerative disease treatment
MeSH terms
Animals, Autophagy, Humans, Lipids, Lysosomes, Parkinson Disease, Pinocytosis, Signal Transduction, Molecular Chaperones, Neurodegenerative Diseases

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review