Evidence map›Paper›PMID 22745480›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012

Neurite sprouting and synapse deterioration in the aging Caenorhabditis elegans nervous system.

Marton Lorant Toth, Ilija Melentijevic, Leena Shah, Aatish Bhatia, Kevin Lu, Amish Talwar, Haaris Naji, Carolina Ibanez-Ventoso, Piya Ghose, Angela Jevince and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers.

0numbers the graph read from it
0cells of the map it votes in
130citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

130 citing papers in PubMed, 217 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Functional Analysis of Late-Onset Alzheimer's Disease Risk Genes inbioRxiv : the preprint server for biology · 2026
    Article
  5. eNeuro · 2026
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Nonapoptotic role of EGL-1 in exopher production and neuronal health inProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  18. Review
  19. Article
  20. Autism candidate genebioRxiv : the preprint server for biology · 2024
    Article

70 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

16 authors at 2 institutions in 2 countries.

Marton Lorant TothDepartment of Molecular Biology and Biochemistry, Nelson Biological Laboratories, Rutgers, The State University of New Jersey, Piscataway, New Jersey 08854, USA.
Ilija Melentijevic
Leena Shah
Aatish Bhatia
Kevin Lu
Amish Talwar
Haaris Naji
Carolina Ibanez-Ventoso
Piya Ghose
Angela Jevince
Jian Xue
Laura A Herndon
Gyan Bhanot
Chris Rongo
David H Hall
Monica Driscoll
Rutgers, The State University of New Jersey · USAlbert Einstein College of Medicine · US

Funding

Center for C elegans AnatomyR24OD010943 · OD · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI DAVID H. HALL, Nathan Schroeder · 2012 to 2026
$9.6M
UMDNJ TRAINING GRANT IN BIOTECHNOLOGYT32GM008339 · NIGMS · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI YARMUSH, MARTIN L · 1989 to 2019
$6.1M
Translational Neuroimaging CoreP30HD071593 · NICHD · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI WALKLEY, STEVEN UPSHAW · 2011 to 2015
$5.6M
MECHANISMS OF DEGENERATIVE CELL DEATH IN C ELEGANSR01NS034435 · NINDS · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI DRISCOLL, MONICA A. · 1995 to 2013
$4.3M
Genetics Analysis of Neuronal Hypoxic Stress ResistanceR01GM101972 · NIGMS · RUTGERS, THE STATE UNIV OF N.J. · PI RONGO, CHRISTOPHER G · 2012 to 2024
$4.1M
Genetics of Sarcopenia &Muscle Healthspan in C.elegansR01AG024882 · NIA · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI DRISCOLL, MONICA A. · 2004 to 2009
$1.9M
Age-associated neuronal sprouting and functional decline in C. elegansR21AG041498 · NIA · RUTGERS, THE STATE UNIV OF N.J. · PI DRISCOLL, MONICA A. · 2011 to 2012
$318k
NIA NIH HHS AG024882NIA NIH HHS R01 AG024882NIA NIH HHS R21 AG041498NICHD NIH HHS HD071593NICHD NIH HHS P30 HD071593NIGMS NIH HHS R01 GM101972NIGMS NIH HHS T32 GM008339NIH HHS OD010943NIH HHS R24 OD010943NINDS NIH HHS NS034435NINDS NIH HHS R01 NS034435
6 · The paper itself

Abstract

Caenorhabditis elegans is a powerful model for analysis of the conserved mechanisms that modulate healthy aging. In the aging nematode nervous system, neuronal death and/or detectable loss of processes are not readily apparent, but because dendrite restructuring and loss of synaptic integrity are hypothesized to contribute to human brain decline and dysfunction, we combined fluorescence microscopy and electron microscopy (EM) to screen at high resolution for nervous system changes. We report two major components of morphological change in the aging C. elegans nervous system: (1) accumulation of novel outgrowths from specific neurons, and (2) physical decline in synaptic integrity. Novel outgrowth phenotypes, including branching from the main dendrite or new growth from somata, appear at a high frequency in some aging neurons, but not all. Mitochondria are often associated with age-associated branch sites. Lowered insulin signaling confers some maintenance of ALM and PLM neuron structural integrity into old age, and both DAF-16/FOXO and heat shock factor transcription factor HSF-1 exert neuroprotective functions. hsf-1 can act cell autonomously in this capacity. EM evaluation in synapse-rich regions reveals a striking decline in synaptic vesicle numbers and a diminution of presynaptic density size. Interestingly, old animals that maintain locomotory prowess exhibit less synaptic decline than same-age decrepit animals, suggesting that synaptic integrity correlates with locomotory healthspan. Our data reveal similarities between the aging C. elegans nervous system and mammalian brain, suggesting conserved neuronal responses to age. Dissection of neuronal aging mechanisms in C. elegans may thus influence the development of brain healthspan-extending therapies.

Indexed as

Age FactorsAgingAnimalsAnimals, Genetically ModifiedCaenorhabditis elegansCaenorhabditis elegans ProteinsForkhead Transcription FactorsGreen Fluorescent ProteinsMicroscopy, Electron, TransmissionMitochondriaMutationNervous SystemNeuritesNeuronsReceptor, InsulinSignal TransductionCaenorhabditis elegans Proteinsdaf-16 protein, C elegansForkhead Transcription FactorsGreen Fluorescent Proteinsheat shock factor-1, C elegansReceptor, InsulinTranscription Factors

Identifiers

PMID22745480
PMCPMC3427745
OpenAlexW2058446462

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.