Evidence map›Paper›PMID 39455560›Full record

ArticleNature communications2024

Accumulation of F-actin drives brain aging and limits healthspan in Drosophila.

Edward T Schmid, Joseph M Schinaman, Naomi Liu-Abramowicz, Kylie S Williams, David W Walker

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–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

22 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Alterations of actin in aging.Journal of cell science · 2026
    Review
  6. Review
  7. Article
  8. ARP2/3 complex mediates the neuropathology of PTEN-deficient human neural cells downstream of mTORC1 and mTORC2 hyperactivation.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Form and function of actin impacts actin health and aging.bioRxiv : the preprint server for biology · 2025
    Article
  14. Neuronal Actin Remodeling and Its Role in Higher Nervous Activity.International journal of molecular sciences · 2025
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Molecular mechanism on autophagy associated cardiovascular dysfunction inFrontiers in cell and developmental biology · 2025
    Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

Edward T SchmidDepartment of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, CA, 90095, USA.
Joseph M SchinamanDepartment of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, CA, 90095, USA.
Naomi Liu-AbramowiczDepartment of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, CA, 90095, USA.
Kylie S WilliamsDepartment of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, CA, 90095, USA.
David W WalkerDepartment of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, CA, 90095, USA. davidwalker@ucla.edu.ORCID 0000-0002-9422-2178

Funding

Resource Component: Acquisition, maintenance and distribution of Drosophila stocksP40OD018537 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Annette L. Parks · 2014 to 2026
$13.5M
Role of Mitochondrial Homeostasis in Animal AgingR01AG037514 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI David W Walker · 2010 to 2026
$5.3M
Role of Intestinal Homeostasis in Organismal Aging.R01AG049157 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WALKER, DAVID W · 2015 to 2025
$2.4M
NIA NIH HHS R01 AG037514NIA NIH HHS R01 AG049157NIH HHS P40 OD018537U.S. Department of Health & Human Services | NIH | National Institute on Aging (U.S. National Institute on Aging) R01AG037514U.S. Department of Health & Human Services | NIH | National Institute on Aging (U.S. National Institute on Aging) RO1AG049157
6 · The paper itself

Abstract

The actin cytoskeleton is a key determinant of cell structure and homeostasis. However, possible tissue-specific changes to actin dynamics during aging, notably brain aging, are not understood. Here, we show that there is an age-related increase in filamentous actin (F-actin) in Drosophila brains, which is counteracted by prolongevity interventions. Critically, decreasing F-actin levels in aging neurons prevents age-onset cognitive decline and extends organismal healthspan. Mechanistically, we show that autophagy, a recycling process required for neuronal homeostasis, is disabled upon actin dysregulation in the aged brain. Remarkably, disrupting actin polymerization in aged animals with cytoskeletal drugs restores brain autophagy to youthful levels and reverses cellular hallmarks of brain aging. Finally, reducing F-actin levels in aging neurons slows brain aging and promotes healthspan in an autophagy-dependent manner. Our data identify excess actin polymerization as a hallmark of brain aging, which can be targeted to reverse brain aging phenotypes and prolong healthspan.

Indexed as

ActinsAgingAutophagyBrainDrosophila melanogasterActin CytoskeletonAnimalsDrosophilaDrosophila ProteinsNeuronsActinsDrosophila Proteins

Identifiers

PMID39455560
PMCPMC11512044

What Socratic 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 Socratic graph.