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OCIAD1 contributes to neurodegeneration in Alzheimer's disease by inducing mitochondria dysfunction, neuronal vulnerability and synaptic damages

EBioMedicine(2020)10.1016/j.ebiom.2019.11.030Source: DataRank Database

OCIAD1 contributes to neurodegeneration in Alzheimer's disease by inducing mitochondria dysfunction, neuronal vulnerability and synaptic damages is a research paper published in EBioMedicine (2020). On theSindex it has a DataRank of 0. It has been cited 18 times.

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0DataRank · unranked

Scored on demand from live citation data

Open Access18 citations

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Linked data & code

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›Methodology & internals

datarank_citation_only_1hop_v6· scope data_onlyMethodology

Pipeline:MetadataData-paper checkEnrichmentCitation networkScoring

Enrichment:Funding (2 grants)Impact (FWCI 1.13)OA: goldTopics (90)IDs (PubMed, PMC, OpenAlex)Annotations (2)SDGs (1)

FAIR Checklist

Context only (not used in score)

Findable (1/2)

Has DOI

Accessible (1/2)

Open Access

Interoperable (0/2)

Reusable (0/3)

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Authors (11)

Lin Wang ORCID,Matthew D. Cykowski ORCID,Tiancheng He ORCID,Timothy Liu ORCID,Joshua Chakranarayan

Live enrichment

PubMed:31931285 PMC:PMC6957876 OpenAlex:https://openalex.org/W2999781629

NIA NIH HHS

Grant: R01 AG057635

National Institutes of Health

Grant: 1R01AG057635-01A1

Systematic Alzheimer's disease drug repositioning (SMART) based on bioinformatics-guided phenotype screening and image-omics

FWCI

1.13

Citation Percentile

0.8%

Citation Trend

2020

2021

2023

2024

2025

2026

goldLicense: cc-by-nc-nd

journalhttp://www.thelancet.com/article/S2352396419307790/pdf

publisherhttp://www.thelancet.com/article/S2352396419307790/pdf

publisherhttps://api.elsevier.com/content/article/PII:S2352396419307790?httpAccept=text/xml

publisherhttps://api.elsevier.com/content/article/PII:S2352396419307790?httpAccept=text/plain

journalhttps://doi.org/10.1016/j.ebiom.2019.11.030

Fields of Study

Alzheimer's disease research and treatmentsTryptophan and brain disordersAmyotrophic Lateral Sclerosis Research03 medical and health sciences0302 clinical medicineAlzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainCaspase 3Cell DeathEnzyme ActivationF-Box ProteinsGlycogen Synthase Kinase 3 betaHumansMembrane Potential, MitochondrialMiceMice, TransgenicMitochondriaNeoplasm ProteinsNerve DegenerationNeuronsProtein AggregatesProtein BindingProto-Oncogene Proteins c-bcl-2SynapsesTumor Suppressor Protein p53Up-Regulation

MeSH Terms

Glycogen Synthase Kinase 3 betaAlzheimer DiseaseAnimalsBrainEnzyme ActivationHumansMice, TransgenicMitochondriaNeoplasm ProteinsNerve DegenerationNeuronsProtein BindingSynapsesUp-RegulationTumor Suppressor Protein p53Amyloid beta-PeptidesCell DeathProto-Oncogene Proteins c-bcl-2F-Box ProteinsMiceMembrane Potential, MitochondrialCaspase 3Protein Aggregates

Keywords

NeurodegenerationNeuroscienceVulnerability (computing)MitochondrionAlzheimer's diseaseDiseaseMedicineBiologyPathologyCell biologyComputer scienceComputer securityMitochondrial DysfunctionOciad1HyperamyloidosisMedicine (General)Research paperMice, TransgenicMiceProtein AggregatesR5-920Alzheimer DiseaseAnimalsHumansMembrane Potential, MitochondrialNeuronsAmyloid beta-PeptidesGlycogen Synthase Kinase 3 betaCell DeathCaspase 3F-Box ProteinsRBrainMitochondriaNeoplasm ProteinsEnzyme ActivationProto-Oncogene Proteins c-bcl-2Nerve DegenerationProtein Binding

Sustainable Development Goals

SDG 3: 3. Good health