Evidence map›Paper›PMID 30293574›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2018

N-methyl-D-aspartate receptor-mediated calcium influx connects amyloid-β oligomers to ectopic neuronal cell cycle reentry in Alzheimer's disease.

Erin J Kodis, Sophie Choi, Eric Swanson, Gonzalo Ferreira, George S Bloom

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
5.6field-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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Advances in the treatment of Alzheimer's disease.Frontiers in pharmacology · 2026
    Review
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  7. Article
  8. Review
  9. Article
  10. Article
  11. Future Perspectives of NMDAR in CNS Disorders.Molecules (Basel, Switzerland) · 2025
    Review
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  13. Review
  14. Article
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  18. Article
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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 2 institutions in 2 countries.

Erin J KodisDepartment of Biology, University of Virginia, Charlottesville, VA, USA. Electronic address: ejk7tj@virginia.edu.
Sophie ChoiDepartment of Biology, University of Virginia, Charlottesville, VA, USA.
Eric SwansonDepartment of Biology, University of Virginia, Charlottesville, VA, USA.
Gonzalo FerreiraDepartamento de Biofisica de la Facultad de Medicina, Universidad de la República, Monetivideo, Uruguay.
George S BloomDepartment of Biology, University of Virginia, Charlottesville, VA, USA; Department of Cell Biology, University of Virginia, Charlottesville, VA, USA; Department of Neuroscience, University of Virginia, Charlottesville, VA, USA. Electronic address: gsb4g@virginia.edu.
University of Virginia · USUniversidad de la República · UY

Funding

Linking Tau Structure to Its Functions and Mechanisms in Alzheimer’s DiseaseRF1AG051085 · NIA · UNIVERSITY OF VIRGINIA · PI BLOOM, GEORGE S · 2016 to 2016
$1.8M
NIA NIH HHS RF1 AG051085
6 · The paper itself

Abstract

introductionAlzheimer's disease (AD) symptoms reflect synaptic dysfunction and neuron death. Amyloid-β oligomers (AβOs) induce excess calcium entry into neurons via N-methyl-D-aspartate receptors (NMDARs), contributing to synaptic dysfunction. The study described here tested the hypothesis that AβO-stimulated calcium entry also drives neuronal cell cycle reentry (CCR), a prelude to neuron death in AD.

methodsPharmacologic modulators of calcium entry and gene expression knockdown were used in cultured neurons and AD model mice.

resultsIn cultured neurons, AβO-stimulated CCR was blocked by NMDAR antagonists, total calcium chelation with 1,2-Bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetrakis(acetoxymethyl ester) (BAPTA-AM), or knockdown of the NMDAR subunit, NR1. NMDAR antagonists also blocked the activation of calcium-calmodulin-dependent protein kinase II and treatment of Tg2576 AD model mice with the NMDAR antagonist, memantine, prevented CCR. DISCUSSION: This study demonstrates a role for AβO-stimulated calcium influx via NMDAR and CCR in AD and suggests the use of memantine as a disease-modifying therapy for presymptomatic AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsCalciumCell CycleCells, CulturedDisease Models, AnimalExcitatory Amino Acid AntagonistsHEK293 CellsHumansIntracellular SpaceMemantineMice, Inbred C57BLMice, TransgenicNeuronsReceptors, N-Methyl-D-AspartateAmyloid beta-PeptidesCalciumExcitatory Amino Acid AntagonistsMemantineReceptors, N-Methyl-D-AspartateAlzheimer's diseaseAmyloid-β oligomersCalciumNeuronal cell cycle reentryNMDA receptorTau

Identifiers

PMID30293574
PMCPMC8363206
OpenAlexW2810261013

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.