ArticleEuropean journal of histochemistry : EJH2019
miR-132 regulates the expression of synaptic proteins in APP/PS1 transgenic mice through C1q.
Article in European journal of histochemistry : EJH, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 42 citations in OpenAlex.
- The complement cascade in Alzheimer's disease: modern implications of an ancient immune protagonist.Molecular neurodegeneration · 2025Review
- MicroRNAs and synaptic dysfunction in Parkinson's disease.Molecular therapy. Nucleic acids · 2025Review
- Epigenetic Dysregulation in Neurodegenerative Disease: Implications for Neuropathology and Therapy.Cureus · 2025Review
- Intracranial self-stimulation mitigates spatial task deficits, modifies miR-146a and miR-495 serum levels and restores hippocampal NRF2 levels in a rat model of sporadic Alzheimer's disease.Frontiers in aging neuroscience · 2025Article
- A Comparative Analysis on Impact of Extraction Methods on Carotenoids Composition, Antioxidants, Antidiabetes, and Antiobesity Properties in SeagrassMarine drugs · 2024Article
- Beneficial effects of miR-132/212 deficiency in the zQ175 mouse model of Huntington's disease.Frontiers in neuroscience · 2024Article
- Non-coding RNAs and neuroinflammation: implications for neurological disorders.Experimental biology and medicine (Maywood, N.J.) · 2024Review
- The role of microRNAs in neurodegenerative diseases: a review.Cell biology and toxicology · 2023Review
- Gene×environment interactions in autism spectrum disorders.Current topics in developmental biology · 2023Review
- MicroRNAs in Learning and Memory and Their Impact on Alzheimer's Disease.Biomedicines · 2022Review
- Histochemistry for nucleic acid research: 60 years in the European Journal of Histochemistry.European journal of histochemistry : EJH · 2022Review
- A bidirectional competitive interaction between circHomer1 and Homer1b within the orbitofrontal cortex regulates reversal learning.Cell reports · 2022Article
- Non-Coding RNAs as Novel Regulators of Neuroinflammation in Alzheimer's Disease.Frontiers in immunology · 2022Review
- microRNA-877-5p exerts tumor-suppressive functions in prostate cancer through repressing transcription of forkhead box M1.Bioengineered · 2021Article
- Diets with Higher ω-6/ω-3 Ratios Show Differences in Ceramides and Fatty Acid Levels Accompanied by Increased Amyloid-Beta in the Brains of Male APP/PS1 Transgenic Mice.International journal of molecular sciences · 2021Article
- SRY-Box 21 Antisense RNA 1 Knockdown Diminishes Amyloid BetaNeurochemical research · 2021Article
- Alzheimer's Disease and microRNA-132: A Widespread Pathological Factor and Potential Therapeutic Target.Frontiers in neuroscience · 2021Review
- The Eminent Role of microRNAs in the Pathogenesis of Alzheimer's Disease.Frontiers in aging neuroscience · 2021Review
- Roles of Exosomes and Exosomal MicroRNAs in Postoperative Sleep Disturbance.Nature and science of sleep · 2021Review
- MicroRNAs as Potential Orchestrators of Alzheimer's Disease-Related Pathologies: Insights on Current Status and Future Possibilities.Frontiers in aging neuroscience · 2021Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cognitive impairment in Alzheimer's disease (AD) is usually accompanied by synaptic loss in both the hippocampus and neocortex. In the early stage of AD, amyloid β-induced synapse changes is the main reason, while in the later stage, the accumulation of Tau protein promotes synapse degeneration as the key factor leading to dementia. MicroRNA (miRNA) is closely related to the expression changes of many AD-related genes. One of the most abundant brain-enriched miRNAs is miR-132, which has been shown to regulate both neuron morphogenesis and plasticity. It has been reported that miR-132 is significantly reduced in the brains of Alzheimer's patients. Genetic deletion of miR-132 in mice promotes Aβ deposition, leading to impaired memory and enhanced Tau pathology, but how the miRNA-mediated gene expression dysregulation contributes to AD pathology remains unclear. Here we found the possible downstream target of miR-132 by in silico analysis, namely C1q. C1q is the primary protein of classical complement cascade, which is highly expressed in the synaptic regions of the central nervous system in Alzheimer's patients. However, it is not clear whether miR-132 plays a role in AD through regulating C1q. To address this question, the APP/PS1 transgenic mice were transfected with miR-132 and given C1 inhibitors. Behavior tests were conducted to assess memory and cognitive abilities seven days after administration. In addition, we analyzed the expression of PSD95, Synapsin-1 and phosphorylated (p)-Synapsin. We found that the expression levels of the synaptic proteins treated with miR-132 or C1INH were significantly increased compared with the AD group. Further RT-qPCR result suggested that miR-132 might regulate C1q expression in AD.
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