Evidence map›Paper›PMID 23821337›Full record

ArticleNeuromolecular medicine2013

Calcineurin inhibition rescues early synaptic plasticity deficits in a mouse model of Alzheimer's disease.

Virve Cavallucci, Nicola Berretta, Annalisa Nobili, Robert Nisticò, Nicola B Mercuri, Marcello D'Amelio

Abstract read
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In one paragraph

Article in Neuromolecular medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

33 citing papers in PubMed, 60 citations in OpenAlex.

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  7. 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
  8. Pin1 and Alzheimer's disease.Translational research : the journal of laboratory and clinical medicine · 2023
    Review
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  12. Article
  13. Synaptic tau: A pathological or physiological phenomenon?Acta neuropathologica communications · 2021
    Review
  14. Calcium Dyshomeostasis in Alzheimer's Disease Pathogenesis.International journal of molecular sciences · 2021
    Review
  15. Review
  16. Review
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  18. Review
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  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

6 authors at 3 institutions in 1 country.

Virve CavallucciDepartment of Experimental Neurosciences, IRCCS Santa Lucia Foundation, Via del Fosso di Fiorano, 64/65, 00143, Rome, Italy.
Nicola Berretta
Annalisa Nobili
Robert Nisticò
Nicola B Mercuri
Marcello D'Amelio
Istituti di Ricovero e Cura a Carattere Scientifico · ITSapienza University of Rome · ITUniversità Campus Bio-Medico · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Functional and ultrastructural investigations support the concept that altered brain connectivity, exhausted neural plasticity, and synaptic loss are the strongest correlates of cognitive decline in age-related neurodegenerative dementia of Alzheimer's type. We have previously demonstrated that in transgenic mice, expressing amyloid-β precursor protein-Swedish mutation active caspase-3 accumulates in hippocampal postsynaptic compartments leading to altered postsynaptic density (PSD) composition, increased long-term depression (LTD), and dendritic spine loss. Furthermore, we found strong evidence that dendritic spine alteration is mediated by calcineurin activation, a calcium-dependent phosphatase involved in synapse signaling. In the present work, we analyzed the molecular mechanism linking alteration of synaptic plasticity to the increase of calcineurin activity. We found that acute treatment of young and plaque-free transgenic mice with the calcineurin inhibitor FK506 leads to a complete rescue of LTD and PSD composition. Our findings are in agreement with other results reporting that calcineurin inhibition improves memory function and restores dendritic spine density, confirming that calcineurin inhibition may be explored as a neuroprotective treatment to stop or slowdown synaptic alterations in Alzheimer's disease.

Indexed as

Calcineurin InhibitorsAlzheimer DiseaseAnimalsCA1 Region, HippocampalCaspase 3DendritesDisease Models, AnimalDisks Large Homolog 4 ProteinDrug Evaluation, PreclinicalExcitatory Postsynaptic PotentialsGuanylate KinasesLong-Term Synaptic DepressionMaleMembrane ProteinsMethoxyhydroxyphenylglycolMice3,4-dihydroxyphenylglycolCalcineurin InhibitorsCasp3 protein, mouseCaspase 3Disks Large Homolog 4 ProteinDlg4 protein, mouseGuanylate KinasesMembrane ProteinsMethoxyhydroxyphenylglycolNeuroprotective AgentsPhosphoserineReceptors, AMPAReceptors, Metabotropic GlutamateTacrolimus

Identifiers

PMID23821337
OpenAlexW1984293506

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.