Evidence map›Paper›PMID 24171818›Full record

ReviewAlzheimer's research & therapy2013

Autophagic/lysosomal dysfunction in Alzheimer's disease.

Miranda E Orr, Salvatore Oddo

Abstract readReview
In one paragraph

Review in Alzheimer's research & therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
118citing papers in PubMed, 2 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

118 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Emerging links between pediatric lysosomal storage diseases and adult parkinsonism.Movement disorders : official journal of the Movement Disorder Society · 2019
    Pooled it
  3. Genetic and molecular evidence linking CTSH to Alzheimer's disease pathophysiology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Enhanced lysosomal activity prevents infection with PrPThe Journal of biological chemistry · 2026
    Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Gaultheria leucocarpa inhibits Aβ fibrillization and enhances mitophagy-mediated degradation of pathogenic proteins.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
  19. Article
  20. Review

58 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.

Miranda E OrrDepartment of Physiology and The Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA.
Salvatore OddoDepartment of Physiology and The Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA ; Banner Sun Health Research Institute and Department of Basic Medical Sciences, University of Arizona College of Medicine-Phoenix, 10515 W. Santa Fe Drive, Sun City, AZ 85351, USA.

Funding

Molecular interplay between Abeta, tau and mTOR: Mechanisms of neurodegenerationR01AG037637 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI ODDO, SALVATORE · 2011 to 2015
$1.6M
NIA NIH HHS R01 AG037637
6 · The paper itself

Abstract

Autophagy serves as the sole catabolic mechanism for degrading organelles and protein aggregates. Increasing evidence implicates autophagic dysfunction in Alzheimer's disease (AD) and other neurodegenerative diseases associated with protein misprocessing and accumulation. Under physiologic conditions, the autophagic/lysosomal system efficiently recycles organelles and substrate proteins. However, reduced autophagy function leads to the accumulation of proteins and autophagic and lysosomal vesicles. These vesicles contain toxic lysosomal hydrolases as well as the proper cellular machinery to generate amyloid-beta, the major component of AD plaques. Here, we provide an overview of current research focused on the relevance of autophagic/lysosomal dysfunction in AD pathogenesis as well as potential therapeutic targets aimed at restoring autophagic/lysosomal pathway function.

Identifiers

PMID24171818
PMCPMC3979020

What OpenQuestion holds

Textmetadata
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.