ArticleAmerican journal of Alzheimer's disease and other dementias
MiR-130a-3p Has Protective Effects in Alzheimer's Disease via Targeting DAPK1.
Article in American journal of Alzheimer's disease and other dementias. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 22 citations in OpenAlex.
- MicroRNA and Alzheimer's disease: Diagnostic biomarkers and potential therapeutic targets.Neural regeneration research · 2026Article
- Crosstalk between death-associated protein kinase 1-regulated mechanisms and dysfunctions in alzheimer's disease.Molecular biology reports · 2026Review
- A Novel PROTAC Confers a Dual Benefit Against Amyloid and Tau Pathology in Alzheimer's Disease via DAPK1 Degradation.International journal of biological sciences · 2026Article
- BMSCs-derived exosomal Egr2 inhibited OGD/R-induced neuronal cell injury through the RNF8/DAPK1 axis in ischemic stroke.Experimental brain research · 2025Article
- In Silico Analysis of s-DAPK-1: From Structure to Function and Regulation.Current issues in molecular biology · 2025Article
- Polyphenols and miRNA interplay: a novel approach to combat apoptosis and inflammation in Alzheimer's disease.Frontiers in aging neuroscience · 2025Review
- Brain microRNA profiles after exposure to heroin in rats.Experimental brain research · 2024Article
- Expression quantitative trait locus mapping of extracellular microRNAs in human plasma.iScience · 2024Article
- Potential Application of MicroRNAs and Some Other Molecular Biomarkers in Alzheimer's Disease.Current issues in molecular biology · 2024Review
- NcRNAs: A synergistically antiapoptosis therapeutic tool in Alzheimer's disease.CNS neuroscience & therapeutics · 2024Review
- MiR-130a-3p inhibits endothelial inflammation by regulating the expression of MAPK8 in endothelial cells.Heliyon · 2024Article
- Death-associated protein kinase 1 as a therapeutic target for Alzheimer's disease.Translational neurodegeneration · 2024Review
- Potential Implications of miRNAs in the Pathogenesis, Diagnosis, and Therapeutics of Alzheimer's Disease.International journal of molecular sciences · 2023Review
- MicroRNA-130a-3p impedes the progression of papillary thyroid carcinoma through downregulation of KPNB1 by targeting PSME3.Endocrine · 2023Article
- Review
- Cerebrospinal fluid microRNAs as potential biomarkers in Alzheimer's disease.Frontiers in aging neuroscience · 2023Review
- The Neuroepigenetic Landscape of Vertebrate and Invertebrate Models of Neurodegenerative Diseases.Epigenetics insights · 2022Review
- Identification of DAPK1 as an autophagy-related biomarker for myotonic dystrophy type 1.Frontiers in genetics · 2022Article
- The Involvement of lncRNA HOTAIR/miR-130a-3p Axis in the Regulation of Voluntary Exercise on Cognition and Inflammation of Alzheimer's Disease.American journal of Alzheimer's disease and other dementiasArticle
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study investigated the role and potential mechanisms of miR-130a-3p in AD. SH-SY5Y cells were treated with Aβ 1-42 to construct AD cell models. APP/PS1 mice were used for the animal experiments. MiR-130a-3p was downregulated in Aβ-induced SH-SY5Y cells. Overexpression of miR-130a-3p attenuates Aβ induced SH-SY5Y cell apoptosis. Low miR-130a-3p expression was detected in the hippocampus tissues of AD mice. The Morris water maze (MWM) results indicated that miR-130a-3p upregulation reduced the escape latency time and increased the time of AD mice spent in the target quadrant. DAPK1 was the target gene of miR-130a-3p. High DAPK1 mRNA level was detected in Aβ treated PC 12 cells and in the hippocampus tissues of AD mice. It was concluded that overexpression of miR-130a-3p may attenuate Aβ-induced neurotoxicity and improve the cognitive function of AD mice via targeting DAPK1.
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Registered trials
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.