ArticleNeuroscience bulletin2013
MicroRNA-98 induces an Alzheimer's disease-like disturbance by targeting insulin-like growth factor 1.
Article in Neuroscience bulletin, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- Pooled it
- ACE2: Friend or Foe in Post-COVID-19 Neurodegeneration?International journal of molecular sciences · 2025Review
- Insulin-Like Growth Factor Signaling in Alzheimer's Disease: Pathophysiology and Therapeutic Strategies.Molecular neurobiology · 2025Review
- Exosomes and non-coding RNAs: bridging the gap in Alzheimer's pathogenesis and therapeutics.Metabolic brain disease · 2025Review
- MicroRNAs as novel biomarkers for the diagnosis and treatment of pediatric diseases.Clinical and experimental pediatrics · 2024Article
- Posttranscriptional Regulation of Insulin Resistance: Implications for Metabolic Diseases.Biomolecules · 2022Review
- Alzheimer's disease is an inherent, natural part of human brain aging: an integrated perspective.Free neuropathology · 2022Article
- Inhibition of Glycogen Synthase Kinase and the Neuroprotective Function of Conjugated ZnO-Osthol Nanoparticles in Alzheimer's Disease.Bioinorganic chemistry and applications · 2022Article
- miRNA Involvement in Cerebral Ischemia-Reperfusion Injury.Frontiers in neuroscience · 2022Review
- Molecular basis of the effect of atorvastatin pretreatment on stem cell therapy in chronic ischemic diseases - critical limb ischemia.Physiological research · 2021Article
- Non-coding RNAs and their bioengineering applications for neurological diseases.Bioengineered · 2021Review
- The Emerging Role of Long Non-Coding RNAs and MicroRNAs in Neurodegenerative Diseases: A Perspective of Machine Learning.Biomolecules · 2021Review
- Review
- The Eminent Role of microRNAs in the Pathogenesis of Alzheimer's Disease.Frontiers in aging neuroscience · 2021Review
- Epigenetic Regulation of Amyloid-beta Metabolism in Alzheimer's Disease.Current medical science · 2020Review
- Can miRNAs Be Considered as Diagnostic and Therapeutic Molecules in Ischemic Stroke Pathogenesis?-Current Status.International journal of molecular sciences · 2020Review
- MicroRNAs Dysregulation and Mitochondrial Dysfunction in Neurodegenerative Diseases.International journal of molecular sciences · 2020Review
- Modulation of MicroRNAs as a Potential Molecular Mechanism Involved in the Beneficial Actions of Physical Exercise in Alzheimer Disease.International journal of molecular sciences · 2020Review
- Circulatory miR-98-5p levels are deregulated during diabetes and it inhibits proliferation and promotes apoptosis by targeting PPP1R15B in keratinocytes.RNA biology · 2020Article
- Bu-Shen-Yi-Sui Capsule, an Herbal Medicine Formula, Promotes Remyelination by Modulating the Molecular Signals via Exosomes in Mice with Experimental Autoimmune Encephalomyelitis.Oxidative medicine and cellular longevity · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by extracellular senile plaques and intracellular neurofibrillary tangles. Many microRNAs (miRs) participate in regulating amyloid β (Aβ) formation and the metabolism of tau protein in the process of AD, and some are up-regulated in AD patients or transgenic models of AD. However, the role of miR-98 in AD remains unclear. Here, we showed that the expression of miR-98 was negatively correlated with the insulin-like growth factor 1 (IGF-1) protein level in APP/PS1 mice. MiR-98 target sites in IGF-1 were confirmed by luciferase assay in HEK293 cells. Overexpression of miR-98 in N2a/APP cells down-regulated the IGF-1 protein level and promoted Aβ production, whereas inhibition of miR-98 in N2a/APP cells up-regulated the IGF-1 protein level and suppressed Aβ production. Furthermore, overexpression of miR-98 in N2a/WT cells increased the phosphorylation of tau, whereas inhibition of miR-98 reduced it. These results suggest that miR-98 increases Aβ formation and tau phosphorylation by inhibiting the translation of IGF-1, which might provide a therapeutic strategy for AD.
Indexed as
Identifiers
What OpenQuestion holds
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.