Evidence map›Paper›PMID 38368936›Full record

ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2024

Endo-lysosomal dysfunction in neurodegenerative diseases: opinion on current progress and future direction in the use of exosomes as biomarkers.

Mathieu Herman, Grace W Randall, Julia L Spiegel, Delphina J Maldonado, Sabrina Simoes

Abstract readReview
In one paragraph

Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

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

  1. Pooled it
  2. HIV-1 gp120-induced lysosomal stress responses are controlled by TRPML1 redox sensors.Redox report : communications in free radical research · 2026
    Article
  3. Review
  4. Shared genetic architecture between DTI-ALPS traits and neurodegenerative diseases.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Proteomic analysis links truncated tau to lysosome motility, autophagy, and endo-lysosomal dysfunction.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  15. Review
  16. Endosomal Mechanisms in Heart Failure Pathophysiology.Current heart failure reports · 2025
    Review
  17. Ultrastructural membrane dynamics of mouse and human cortical synapses.bioRxiv : the preprint server for biology · 2025
    Article
  18. Review
  19. Review
  20. Review
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

5 authors.

Mathieu HermanTaub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University Irving Medical Center, New York, NY 10032, USA.
Grace W RandallTaub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University Irving Medical Center, New York, NY 10032, USA.
Julia L SpiegelTaub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University Irving Medical Center, New York, NY 10032, USA.
Delphina J MaldonadoTaub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University Irving Medical Center, New York, NY 10032, USA.
Sabrina SimoesTaub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University Irving Medical Center, New York, NY 10032, USA.ORCID 0000-0002-9976-2501

Funding

Research Education CoreP30AG066462 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI PHILIP L DE JAGER · 2020 to 2026
$30.1M
Targeting Endosomal dysfunction as a new source of biomarkers for Alzheimer's diseaseR01AG071868 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Sabrina Alves Simoes Spassov · 2022 to 2026
$2.2M
Endosomal dysfunction, a new source of biomarkers for Alzheimer's disease.R21AG070768 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI ALVES SIMOES SPASSOV, SABRINA · 2021 to 2022
$446k
NIA NIH HHS P30 AG066462NIA NIH HHS R01 AG071868NIA NIH HHS R21 AG070768
6 · The paper itself

Abstract

Over the past two decades, increased research has highlighted the connection between endosomal trafficking defects and neurodegeneration. The endo-lysosomal network is an important, complex cellular system specialized in the transport of proteins, lipids, and other metabolites, essential for cell homeostasis. Disruption of this pathway is linked to a wide range of neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's disease and frontotemporal dementia. Furthermore, there is strong evidence that defects in this pathway create opportunities for diagnostic and therapeutic intervention. In this

Indexed as

Alzheimer DiseaseExosomesNeurodegenerative DiseasesBiomarkersHumansLysosomesBiomarkersbiomarkersendo-lysosomal dysfunctionendo-lysosomal systemexosomesextracellular vesiclesneurodegenerative diseases

Identifiers

PMID38368936
PMCPMC10874701

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.