Evidence map›Paper›PMID 19641109›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009

Deviant ryanodine receptor-mediated calcium release resets synaptic homeostasis in presymptomatic 3xTg-AD mice.

Shreaya Chakroborty, Ivan Goussakov, Megan B Miller, Grace E Stutzmann

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers.

0numbers the graph read from it
0cells of the map it votes in
136citing papers in PubMed
6.5field-weighted citation impact, top 2% 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

136 citing papers in PubMed, 205 citations in OpenAlex.

  1. Article
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  5. Neuronal Calcium Signaling and Cytoskeletal Dynamics in Neurodegeneration.International journal of molecular sciences · 2026
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  8. Article
  9. Article
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  11. Article
  12. Organelle abnormalities in Alzheimer's disease.Organelle (Tucson, Ariz.) · 2025
    Article
  13. Review
  14. Article
  15. Article
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  17. Synaptopodin: a key regulator of Hebbian plasticity.Frontiers in cellular neuroscience · 2024
    Review
  18. Cytosolic calcium: Judge, jury and executioner of neurodegeneration in Alzheimer's disease and beyond.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023
    Review
  19. Article
  20. Review

76 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

4 authors at 1 institution in 1 country.

Shreaya ChakrobortyDepartment of Neuroscience, Rosalind Franklin University, The Chicago Medical School, North Chicago, Illinois 60064, USA.
Ivan Goussakov
Megan B Miller
Grace E Stutzmann
Rosalind Franklin University of Medicine and Science · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Presenilin mutations result in exaggerated endoplasmic reticulum (ER) calcium release in cellular and animal models of Alzheimer's disease (AD). In this study, we examined whether dysregulated ER calcium release in young 3xTg-AD neurons alters synaptic transmission and plasticity mechanisms before the onset of histopathology and cognitive deficits. Using electrophysiological recordings and two-photon calcium imaging in young (6-8 weeks old) 3xTg-AD and non-transgenic (NonTg) hippocampal slices, we show a marked increase in ryanodine receptor (RyR)-evoked calcium release within synapse-dense regions of CA1 pyramidal neurons. In addition, we uncovered a deviant contribution of presynaptic and postsynaptic ryanodine receptor-sensitive calcium stores to synaptic transmission and plasticity in 3xTg-AD mice that is not present in NonTg mice. As a possible underlying mechanism, the RyR2 isoform was found to be selectively increased more than fivefold in the hippocampus of 3xTg-AD mice relative to the NonTg controls. These novel findings demonstrate that 3xTg-AD CA1 neurons at presymptomatic ages operate under an aberrant, yet seemingly functional, calcium signaling and synaptic transmission system long before AD histopathology onset. These early signaling alterations may underlie the later synaptic breakdown and cognitive deficits characteristic of later stage AD.

Indexed as

Alzheimer DiseaseAnimalsCalciumDisease Models, AnimalEndoplasmic ReticulumHippocampusHumansIn Vitro TechniquesMiceMice, TransgenicNeuronal PlasticityProtein IsoformsPyramidal CellsReceptor, Adenosine A1RNA, MessengerRyanodine Receptor Calcium Release ChannelCalciumProtein IsoformsReceptor, Adenosine A1RNA, MessengerRyanodine Receptor Calcium Release Channel

Identifiers

PMID19641109
PMCPMC6666542
OpenAlexW2072972685

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.