ArticleEMBO molecular medicine2016
miR-132 loss de-represses ITPKB and aggravates amyloid and TAU pathology in Alzheimer's brain.
Article in EMBO molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers, 3 of them syntheses that pooled it.
What it found
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Who cites it
111 citing papers in PubMed, 3 syntheses or guidelines pooled it, 171 citations in OpenAlex.
- Alzheimer's disease large-scale gene expression portrait identifies exercise as the top theoretical treatment.Scientific reports · 2022Pooled it
- Brain microRNAs are associated with variation in cognitive trajectory in advanced age.Translational psychiatry · 2022Pooled it
- Prediction of differentially expressed microRNAs in blood as potential biomarkers for Alzheimer's disease by meta-analysis and adaptive boosting ensemble learning.Alzheimer's research & therapy · 2021Pooled it
- Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer's disease.Ageing research reviews · 2026Review
- MicroRNA and Alzheimer's disease: Diagnostic biomarkers and potential therapeutic targets.Neural regeneration research · 2026Article
- Exercise mimetics: molecular mechanisms, biological and therapeutic effects.Molecular biomedicine · 2026Review
- Genetic drivers of progression in Alzheimer's disease are distinct from disease risk.Alzheimer's research & therapy · 2026Article
- microRNA-132 attenuates inflammation in induced pluripotent stem cell-derived microglia from Alzheimer's disease patients.Acta neuropathologica communications · 2026Article
- Morpho-Functional Characterization and miRNA Profiling of the Retina in the 5xFAD Murine Model of Alzheimer's Disease.Investigative ophthalmology & visual science · 2026Article
- Sub-Neuronal Network Profiling of Extracellular Vesicle Release Using a Compartmentalized Neurofluidic Platform.Advanced biology · 2026Article
- Differentially expressed miRNAs in the temporal cortex of Alzheimer's disease patients and their association to tau pathology.Communications biology · 2026Article
- Exercise-conditioned extracellular vesicles in Alzheimer's disease: a multi-organ signaling network linking peripheral adaptation to brain pathology.Frontiers in immunology · 2026Review
- Modulatory potential of A novel benzofuran-derived compound against aluminium chloride-induced neurotoxicity and miRNA dysregulation: Biochemical and bio-analytical study.Toxicology reports · 2025Article
- Review
- miR-132 and Its Exosomal Form in Alzheimer's Disease: Linking Epigenetic Regulation to Neurodegeneration.Molecular neurobiology · 2025Review
- The Ubiquitin-Proteasome System in Brain Disorders: Pathogenic Pathways, Post-Translational Tweaks, and Therapeutic Frontiers.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Review
- Genetic drivers of progression in Alzheimer's disease are distinct from disease risk.medRxiv : the preprint server for health sciences · 2025Article
- The emerging role of miRNAs in biological aging and age-related diseases.Non-coding RNA research · 2025Review
- The neuroinflammatory role of microRNAs in Alzheimer's disease: pathological insights to therapeutic potential.Molecular and cellular biochemistry · 2025Review
- A role for astrocytic miR-129-5p in frontotemporal dementia.Translational psychiatry · 2025Article
51 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
microRNA-132 (miR-132) is involved in prosurvival, anti-inflammatory and memory-promoting functions in the nervous system and has been found consistently downregulated in Alzheimer's disease (AD). Whether and how miR-132 deficiency impacts AD pathology remains, however, unaddressed. We show here that miR-132 loss exacerbates both amyloid and TAU pathology via inositol 1,4,5-trisphosphate 3-kinase B (ITPKB) upregulation in an AD mouse model. This leads to increased ERK1/2 and BACE1 activity and elevated TAU phosphorylation. We confirm downregulation of miR-132 and upregulation of ITPKB in three distinct human AD patient cohorts, indicating the pathological relevance of this pathway in AD.
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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.