ArticleFrontiers in aging neuroscience2016
Over-Expressed Pathogenic miRNAs in Alzheimer's Disease (AD) and Prion Disease (PrD) Drive Deficits in TREM2-Mediated Aβ42 Peptide Clearance.
Article in Frontiers in aging neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- Systematic review of bidirectional interaction between gut microbiome, miRNAs, and human pathologies.Frontiers in microbiology · 2025Pooled it
- TREM2 in neurodegenerative diseases and acute neurological injuries: mechanisms to targeted therapies.Cell communication and signaling : CCS · 2026Review
- The role of peripheral blood microRNAs in the pathogenesis and treatment response of age-related macular degeneration.Future science OA · 2025Review
- Apolipoprotein E dysfunction in Alzheimer's disease: a study on miRNA regulation, glial markers, and amyloid pathology.Frontiers in aging neuroscience · 2024Article
- MicroRNA (miRNA) Complexity in Alzheimer's Disease (AD).Biology · 2023Review
- Extracellular Vesicles, Stem Cells and the Role of miRNAs in Neurodegeneration.Current neuropharmacology · 2022Review
- Prediction of P-tau/Aβ42 in the cerebrospinal fluid with blood microRNAs in Alzheimer's disease.BMC medicine · 2021Article
- RNA Dynamics in Alzheimer's Disease.Molecules (Basel, Switzerland) · 2021Review
- Unravelling the potential of gut microbiota in sustaining brain health and their current prospective towards development of neurotherapeutics.Archives of microbiology · 2021Review
- Gastrointestinal (GI)-Tract Microbiome Derived Neurotoxins and their Potential Contribution to Inflammatory Neurodegeneration in Alzheimer's Disease (AD).Journal of Alzheimer's disease & Parkinsonism · 2021Article
- Biomarkers for Alzheimer's Disease (AD) and the Application of Precision Medicine.Journal of personalized medicine · 2020Article
- Vesicular Transport of Encapsulated microRNA between Glial and Neuronal Cells.International journal of molecular sciences · 2020Review
- MicroRNA-34a Acutely Regulates Synaptic Efficacy in the Adult Dentate Gyrus In Vivo.Molecular neurobiology · 2020Article
- MicroRNA-146a Is a Wide-Reaching Neuroinflammatory Regulator and Potential Treatment Target in Neurological Diseases.Frontiers in molecular neuroscience · 2020Article
- RNA and Oxidative Stress in Alzheimer's Disease: Focus on microRNAs.Oxidative medicine and cellular longevity · 2020Review
- Microbiome Influence in the Pathogenesis of Prion and Alzheimer's Diseases.International journal of molecular sciences · 2019Review
- Curcumin restores innate immune Alzheimer's disease risk gene expression to ameliorate Alzheimer pathogenesis.Neurobiology of disease · 2019Article
- Imbalance of Microglial TLR4/TREM2 in LPS-Treated APP/PS1 Transgenic Mice: A Potential Link Between Alzheimer's Disease and Systemic Inflammation.Neurochemical research · 2019Article
- The cell type resolved mouse transcriptome in neuron-enriched brain tissues from the hippocampus and cerebellum during prion disease.Scientific reports · 2019Article
- MicroRNAs in Alzheimer's Disease.Frontiers in genetics · 2019Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
One prominent and distinguishing feature of progressive, age-related neurological diseases such as Alzheimer's disease (AD) and prion disease (PrD) is the gradual accumulation of amyloids into dense, insoluble end-stage protein aggregates. These polymorphic proteolipid lesions are known to contribute to immunogenic and inflammatory pathology in these insidious and fatal disorders of the human central nervous system (CNS). For example, the evolution of self-aggregating amyloid-beta (Aβ) peptides, such as the 42 amino acid Aβ42 peptide monomer into higher order aggregates are largely due to: (1) the inability of natural processes to clear them from the cellular environment; and/or (2) the overproduction of these amyloid monomers which rapidly mature into higher order oligomers, fibrils and insoluble, end-stage senile plaques. Cells of the CNS such as microglial (MG) cells have evolved essential homeostatic mechanisms to clear Aβ peptides to avoid their accumulation, however, when defective, these clearance mechanisms become overwhelmed and excessive deposition and aggregation of these amyloids result. This 'Perspectives' paper will highlight some emerging concepts on the up-regulation of an inducible microRNA-34a in AD and PrD that drives the down-regulation of the amyloid sensing- and clearance receptor protein TREM2 (the triggering receptor expressed in myeloid/microglial cells). The impairment of this inducible, miRNA-34a-regulated TREM2- and MG-cell based amyloid clearance mechanism may thereby contribute to the age-related amyloidogenesis associated with both AD and PrD.
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Registered trials
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