Evidence map›Paper›PMID 26603284›Full record

ReviewMolecular brain2015

Calcium/calmodulin-dependent kinase II and Alzheimer's disease.

Anshua Ghosh, Karl Peter Giese

Abstract readReview
In one paragraph

Review in Molecular brain, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

112 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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52 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

2 authors.

Anshua GhoshMaurice Wohl Clinical Neuroscience Institute, King's College London, 5 Cutcombe Road, London, SE5 9RT, UK. anshua.ghosh@kcl.ac.uk.
Karl Peter GieseMaurice Wohl Clinical Neuroscience Institute, King's College London, 5 Cutcombe Road, London, SE5 9RT, UK. karl.giese@kcl.ac.uk.

Funding

Medical Research Council G0800393
6 · The paper itself

Abstract

CaMKII is a remarkably complex protein kinase, known to have a fundamental role in synaptic plasticity and memory formation. Further, CaMKII has also been suggested to be a tau kinase. CaMKII dysregulation may therefore be a modulator of toxicity in Alzheimer's disease, a dementia characterised by aberrant calcium signalling, synapse and neuronal loss, and impaired memory. Here, we first examine the evidence for CaMKII dysregulation in Alzheimer's patients and draw parallels to findings in disease models which recapitulate key aspects of the disease. We then put forward the hypothesis that these changes critically contribute to neurodegeneration and memory impairment in Alzheimer's disease.

Indexed as

Alzheimer DiseaseAnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Disease Models, AnimalHumansModels, BiologicalCalcium-Calmodulin-Dependent Protein Kinase Type 2

Identifiers

PMID26603284
PMCPMC4657223

What OpenQuestion holds

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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.