ArticleInternational journal of molecular sciences2018
miRNA-34c Overexpression Causes Dendritic Loss and Memory Decline.
Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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.
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Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- Epigenetic Basis of Stress-Induced Central Nervous System Disorders: Therapeutic Approaches.Biology · 2026Review
- Neurovascular Impairment in Type 2 Diabetes Mellitus: The Role of Adipocyte-Derived Exosomes.Biomolecules · 2026Review
- miRNAs: Promising Biomarkers for Alzheimer's Diagnosis and Treatment.Current Alzheimer research · 2026Review
- Analysis of Differential microRNA Expression in the Hippocampus of Scopolamine-Induced Amnesic Mouse Model.Molecular neurobiology · 2025Article
- Therapeutic potential and microRNA regulating properties of phytochemicals in Alzheimer's disease.Molecular therapy. Nucleic acids · 2025Review
- Small Differences and Big Changes: The Many Variables of MicroRNA Expression and Function in the Brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Review
- MicroRNAs as biomarkers of brain injury in neonatal encephalopathy: an observational cohort study.Scientific reports · 2024Observational
- MicroRNAs dysregulated in multiple sclerosis affect the differentiation of CG-4 cells, an oligodendrocyte progenitor cell line.Frontiers in cellular neuroscience · 2024Article
- MicroRNAs in Learning and Memory and Their Impact on Alzheimer's Disease.Biomedicines · 2022Review
- The Potential Role of miRNA-Regulated Autophagy in Alzheimer's Disease.International journal of molecular sciences · 2022Review
- Advances in the development of new biomarkers for Alzheimer's disease.Translational neurodegeneration · 2022Review
- Structural Plasticity of the Hippocampus in Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- Let-7c increases BACE2 expression by RNAa and decreases Aβ production.American journal of translational research · 2022Article
- MicroRNA Alterations in Chronic Traumatic Encephalopathy and Amyotrophic Lateral Sclerosis.Frontiers in neuroscience · 2022Article
- MicroRNA-34a Regulates the Depression-like Behavior in Mice by Modulating the Expression of Target Genes in the Dorsal Raphè.Molecular neurobiology · 2020Article
- Impact of Expression and Genetic Variation of microRNA-34b/c on Cognitive Dysfunction in Patients with Major Depressive Disorder.Neuropsychiatric disease and treatment · 2020Article
- MicroRNAs in Alzheimer's Disease: Function and Potential Applications as Diagnostic Biomarkers.Frontiers in molecular neuroscience · 2020Review
- Applications of Acupuncture Therapy in Modulating the Plasticity of Neurodegenerative Disease and Depression: Do MicroRNA and Neurotrophin BDNF Shed Light on the Underlying Mechanism?Neural plasticity · 2020Review
- MicroRNAs in Alzheimer's Disease: Diagnostic Markers or Therapeutic Agents?Frontiers in pharmacology · 2019Review
- Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microribonucleic acids (miRNAs) play a pivotal role in numerous aspects of the nervous system and are increasingly recognized as key regulators in neurodegenerative diseases. This study hypothesized that miR-34c, a miRNA expressed in mammalian hippocampi whose expression level can alter the hippocampal dendritic spine density, could induce memory impairment akin to that of patients with Alzheimer's disease (AD) in mice. In this study, we showed that miR-34c overexpression in hippocampal neurons negatively regulated dendritic length and spine density. Hippocampal neurons transfected with miR-34c had shorter dendrites on average and fewer filopodia and spines than those not transfected with miR-34c (control mice). Because dendrites and synapses are key sites for signal transduction and fundamental structures for memory formation and storage, disrupted dendrites can contribute to AD. Therefore, we supposed that miR-34c, through its effects on dendritic spine density, influences synaptic plasticity and plays a key role in AD pathogenesis.
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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.