Evidence map›Paper›PMID 20157256›Full record

ArticleJournal of Alzheimer's disease : JAD2010

Progressive age-related impairment of the late long-term potentiation in Alzheimer's disease presenilin-1 mutant knock-in mice.

Alexandra Auffret, Vanessa Gautheron, Mark P Mattson, Jean Mariani, Catherine Rovira

Open access · greenAbstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

34 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Review
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  6. Article
  7. Review
  8. Identification of a RareFrontiers in psychiatry · 2020
    Article
  9. Bax inhibitor 1 is a γ-secretase-independent presenilin-binding protein.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  10. Article
  11. Review
  12. Presenilin1/γ-secretase protects neurons from glucose deprivation-induced death by regulating miR-212 and PEA15.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Article
  13. Article
  14. Store-Operated Calcium Channel Complex in Postsynaptic Spines: A New Therapeutic Target for Alzheimer's Disease Treatment.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  15. Article
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  19. Review
  20. Article
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 at 4 institutions in 2 countries.

Alexandra AuffretUniversité Pierre et Marie Curie-Paris6, Centre National de la Recherche Scientifique, UMR 7102-NPA, Paris, France. alexandra.auffret@gmail.com
Vanessa Gautheron
Mark P Mattson
Jean Mariani
Catherine Rovira
Centre National de la Recherche Scientifique · FRHôpital Charles-Foix · FRNational Institute on Aging · USSorbonne Université · FR

Funding

Synaptic Plasticity In Aging And Neurodegenerative DisordersZIAAG000317 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$8.5M
Cellular And Molecular Pathogenesis Of Alzheimer's DiseaseZIAAG000312 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$6.4M
Cellular And Molecular Pathogenesis Of Alzheimer'sZ01AG000312 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK P · 2001 to 2008
$1.9M
Intramural NIH HHS Z01 AG000312
6 · The paper itself

Abstract

Presenilin 1 (PS1) mutations are responsible for many early-onset familial Alzheimer's disease (FAD) cases. While increasing evidence points to impaired synaptic plasticity as an early event in AD, PS1 mutant mice exhibit a paradoxical increase in hippocampal long-term potentiation (LTP). Among PS1 mouse models, PS1 M146V mutant knock-in mice (PS1KI) are particularly interesting in that they exhibit memory impairment in spatial tasks. Here we investigated the effects of aging on two forms of LTP in PS1KI mice, the widely-studied early phase of LTP (E-LTP) and a particular form of LTP called late-LTP (L-LTP) which requires transcription and protein synthesis. L-LTP is thought to be critical for long-term memory. We found a lower L-LTP maintenance phase in PS1KI mice compared to wild type littermates at 3 months of age. As the mice age, they exhibit impairment of both the induction and maintenance phases of LTP. When E-LTP and NMDA receptor-mediated transmission were analyzed, PS1KI mice displayed an increase at 3 months compared to wild type littermates; this difference did not persist at older ages and finally decreased at 12 months. These results reveal an L-LTP decrease in PS1 mutant mice at an early stage, which occurs coincidently with a paradoxical enhancement of E-LTP. The observation of a decrease in both forms of LTP during aging supports the view that PS1KI mice are a valuable model for the study of age-dependent synaptic dysfunction and cognitive decline in AD.

Indexed as

AgingAlzheimer DiseaseAnimalsBrainDisease ProgressionHippocampusLong-Term PotentiationMiceMice, Mutant StrainsPoint MutationPresenilin-1Presenilin-1

Identifiers

PMID20157256
PMCPMC2891870
OpenAlexW1536472139

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.