Evidence map›Paper›PMID 35034773›Full record

ReviewTrends in neurosciences2022

Lysosomal dysfunction in neurodegeneration: emerging concepts and methods.

Vinod Udayar, Yu Chen, Ellen Sidransky, Ravi Jagasia

Open access · greenAbstract readReview
In one paragraph

Review in Trends in neurosciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
144citing papers in PubMed, 1 pooled it
21.9field-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

144 citing papers in PubMed, 1 synthesis or guideline pooled it, 198 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Intra-CNS AAV9-Molecular therapy. Advances · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Neurodegenerative Diseases in Children: A Comprehensive Review.International journal of molecular sciences · 2026
    Review
  15. Article
  16. Small heat shock proteins and biomolecular condensates.Cellular and molecular life sciences : CMLS · 2026
    Review
  17. Review
  18. Article
  19. Article
  20. Article

84 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

4 authors at 3 institutions in 2 countries.

Vinod UdayarRoche Pharmaceutical Research and Early Development, Neuroscience and Rare Diseases Discovery & Translational Area, Roche Innovation Center Basel, F. Hoffmann-La Roche Ltd., Basel, Switzerland.
Yu ChenMedical Genetics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA.
Ellen SidranskyMedical Genetics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA. Electronic address: sidranse@mail.nih.gov.
Ravi JagasiaRoche Pharmaceutical Research and Early Development, Neuroscience and Rare Diseases Discovery & Translational Area, Roche Innovation Center Basel, F. Hoffmann-La Roche Ltd., Basel, Switzerland. Electronic address: ravi.jagasia@roche.com.
Roche (Switzerland) · CHNational Human Genome Research Institute · USNational Institutes of Health · US

Funding

Genetic and clinical studies of Gaucher disease and other lysosomal disordersZIAHG200336 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI SIDRANSKY, ELLEN · 2009 to 2025
$45.2M
Intramural NIH HHS Z99 HG999999
6 · The paper itself

Abstract

The understanding of lysosomes has come a long way since the initial discovery of their role in degrading cellular waste. The lysosome is now recognized as a highly dynamic organelle positioned at the crossroads of cell signaling, transcription, and metabolism. Underscoring its importance is the observation that, in addition to rare monogenic lysosomal storage disorders, genes regulating lysosomal function are implicated in common sporadic neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS). Developing therapies for these disorders is particularly challenging, largely due to gaps in knowledge of the underlying molecular and cellular processes. In this review, we discuss technological advances that have propelled deeper understanding of the lysosome in neurodegeneration, from elucidating the functions of lysosome-related disease risk variants at the level of the organelle, cell, and tissue, to the development of disease-specific biological models that recapitulate disease manifestations. Finally, we identify key questions to be addressed to successfully bridge the gap to the clinic.

Indexed as

Alzheimer DiseaseAmyotrophic Lateral SclerosisParkinson DiseaseHumansLysosomesAlzheimer’s diseaseamyotrophic lateral sclerosisfrontotemporal dementialysosomesParkinson’s disease

Identifiers

PMID35034773
PMCPMC8854344
OpenAlexW4205593204

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.