Evidence map›Paper›PMID 36514335›Full record

ReviewComputational and structural biotechnology journal2023

Modulation of L-type calcium channels in Alzheimer's disease: A potential therapeutic target.

Chelsea A Crossley, Vishaal Rajani, Qi Yuan

Open access · goldAbstract readReview
In one paragraph

Review in Computational and structural biotechnology journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

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  5. Amyloid β alters vascular CaThe Journal of physiology · 2025
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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

3 authors at 1 institution in 1 country.

Chelsea A CrossleyBiomedical Sciences, Faculty of Medicine, Memorial University, Canada.
Vishaal RajaniBiomedical Sciences, Faculty of Medicine, Memorial University, Canada.
Qi YuanBiomedical Sciences, Faculty of Medicine, Memorial University, Canada.
Memorial University of Newfoundland · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calcium plays a fundamental role in various signaling pathways and cellular processes in the human organism. In the nervous system, voltage-gated calcium channels such as L-type calcium channels (LTCCs) are critical elements in mediating neurotransmitter release, synaptic integration and plasticity. Dysfunction of LTCCs has been implicated in both aging and Alzheimer's Disease (AD), constituting a key component of calcium hypothesis of AD. As such, LTCCs are a promising drug target in AD. However, due to their structural and functional complexity, the mechanisms by which LTCCs contribute to AD are still unclear. In this review, we briefly summarize the structure, function, and modulation of LTCCs that are the backbone for understanding pathological processes involving LTCCs. We suggest targeting molecular pathways up-regulating LTCCs in AD may be a more promising approach, given the diverse physiological functions of LTCCs and the ineffectiveness of LTCC blockers in clinical studies.

Indexed as

AC, adenylyl cyclaseAD, Alzheimer’s DiseaseAgingAHP, afterhyperpolarizationAlzheimer’s diseaseAR, adrenoceptorAβ, β-amyloidBIN1, bridging integrator 1BTZs, benzothiazepinesCaMKII, calmodulin-dependent protein kinase IICDF, calcium-dependent facilitationCDI, calcium-dependent inactivationDHP, dihydropyridineLTCC, L-type calcium channelsLTD, long-term depressionLTP, long-term potentiationL-type calcium channelNFT, neurofibrillary tanglesNMDAR, N-methyl-D-aspartate receptorPAA, phenylalkylaminesPKA, protein kinase APKC, protein kinase CPKG, protein kinase GSFK, Src family kinaseTauVSD, voltage sensing domainβ-Amyloid

Identifiers

PMID36514335
PMCPMC9719069
OpenAlexW4310018535

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.