Evidence map›Paper›PMID 10841577›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2000

Alzheimer-like neurodegeneration in aged antinerve growth factor transgenic mice.

S Capsoni, G Ugolini, A Comparini, F Ruberti, N Berardi, A Cattaneo

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 3% 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

99 citing papers in PubMed, 1 synthesis or guideline pooled it, 280 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Therapeutic modulation of neurogenesis to improve hippocampal plasticity and cognition in aging and Alzheimer's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  4. Article
  5. Antigen-specific age-related memory CD8 T cells induce and track Alzheimer's-like neurodegeneration.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  6. Article
  7. Review
  8. Article
  9. Frontiers in psychiatry · 2023
    Review
  10. Reduced levels of NGF shift astrocytes toward a neurotoxic phenotype.Frontiers in cell and developmental biology · 2023
    Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

39 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

6 authors at 1 institution in 1 country.

S CapsoniNeuroscience Program, International School for Advanced Studies, SISSA, Via Beirut 2/4, 34014 Trieste, Italy.
G Ugolini
A Comparini
F Ruberti
N Berardi
A Cattaneo
Scuola Internazionale Superiore di Studi Avanzati · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurotrophin nerve growth factor (NGF) has been suggested to be involved in age-related neurodegenerative diseases, but no transgenic model is currently available to study this concept. We have obtained transgenic mice expressing a neutralizing anti-NGF recombinant antibody, in which the levels of antibodies are three orders of magnitude higher in adult than in newborn mice [F.R., S. C. , A.C., E. Di Daniel, J. Franzot, S. Gonfloni, G. Rossi, N. B. & A. C. (2000) J. Neurosci., 20, 2589-2601]. In this paper, we analyze the phenotype of aged anti-NGF transgenic mice and demonstrate that these mice acquire an age-dependent neurodegenerative pathology including amyloid plaques, insoluble and hyperphosphorylated tau, and neurofibrillary tangles in cortical and hippocampal neurons. Aged anti-NGF mice also display extensive neuronal loss throughout the cortex, cholinergic deficit in the basal forebrain, and behavioral deficits. The overall picture is strikingly reminiscent of human Alzheimer's disease. Aged anti-NGF mice represent, to our knowledge, the most comprehensive animal model for this severe neurodegenerative disease. Also, these results demonstrate that, in mice, a deficit in the signaling and/or transport of NGF leads to neurodegeneration.

Indexed as

AgingAlzheimer DiseaseAnimalsAntibodiesBrainCholine O-AcetyltransferaseCognition DisordersDNA FragmentationHumansMemory DisordersMiceMice, TransgenicNerve Growth FactorParasympathetic Nervous SystemPhosphorylationAntibodiesCholine O-AcetyltransferaseNerve Growth Factor

Identifiers

PMID10841577
PMCPMC18754
OpenAlexW2102367498

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.