ArticleMolecular neurobiology2020
Selected microRNAs Increase Synaptic Resilience to the Damaging Binding of the Alzheimer's Disease Amyloid Beta Oligomers.
Article in Molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Asymptomatic Versus Symptomatic Alzheimer's Disease Neuropathology: A Systematic Review of Differences Reported in Post-Mortem Studies.Neuropathology and applied neurobiology · 2026Pooled it
- Hippocampal neural stem cell-derived extracellular vesicles modulate microglia to promote resilience against tau oligomers.Neural regeneration research · 2026Article
- A Novel Nogo-A Receptor Antagonist Peptide Impedes Alzheimer's Disease Pathology by Nogo-A/NgR/ROCK Signaling Pathway.CNS neuroscience & therapeutics · 2026Article
- Amyloid-β and Tau in Alzheimer's disease: pathogenesis, mechanisms, and interplay.Cell death & disease · 2026Review
- TREM2 and microglial immunity in Alzheimer's disease: mechanisms, genetics, and therapeutic opportunities.Frontiers in immunology · 2026Review
- MicroRNAs in neurodegenerative diseases: from molecular mechanisms to clinical biomarkers, detection methods and therapeutic strategies-advances and challenges.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Review
- Synapse vulnerability and resilience across the clinical spectrum of dementias.Nature reviews. Neurology · 2025Review
- Amyloid-β oligomers increase the binding and internalization of tau oligomers in human synapses.Acta neuropathologica · 2024Article
- The concept of resilience to Alzheimer's Disease: current definitions and cellular and molecular mechanisms.Molecular neurodegeneration · 2024Review
- TREM2-induced activation of microglia contributes to synaptic integrity in cognitively intact aged individuals with Alzheimer's neuropathology.Brain pathology (Zurich, Switzerland) · 2023Article
- Synaptosome microRNAs regulate synapse functions in Alzheimer's disease.NPJ genomic medicine · 2022Article
- Biological aging processes underlying cognitive decline and neurodegenerative disease.The Journal of clinical investigation · 2022Review
- Regulation of Cdc42 signaling by the dopamine D2 receptor in a mouse model of Parkinson's disease.Aging cell · 2022Article
- Aβ/tau oligomer interplay at human synapses supports shifting therapeutic targets for Alzheimer's disease.Cellular and molecular life sciences : CMLS · 2022Article
- Epigenetics in Alzheimer's Disease.Frontiers in aging neuroscience · 2022Review
- Potential Mechanisms Underlying Resistance to Dementia in Non-Demented Individuals with Alzheimer's Disease Neuropathology.Journal of Alzheimer's disease : JAD · 2022Review
- The Food Additive β-Caryophyllene Exerts Its Neuroprotective Effects Through the JAK2-STAT3-BACE1 Pathway.Frontiers in aging neuroscience · 2022Article
- Trilobatin Alleviates Cognitive Deficits and Pathologies in an Alzheimer's Disease Mouse Model.Oxidative medicine and cellular longevity · 2021Article
- Roles and Mechanisms of Gut Microbiota in Patients With Alzheimer's Disease.Frontiers in aging neuroscience · 2021Review
- Personalizing the Care and Treatment of Alzheimer's Disease: An Overview.Pharmacogenomics and personalized medicine · 2021Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is marked by synaptic loss (at early stages) and neuronal death (at late stages). Amyloid beta (Aβ) and tau oligomers can target and disrupt synapses thus driving cognitive decay. Non-demented individuals with Alzheimer's neuropathology (NDAN) are capable of withstanding Aβ and tau toxicity, thus remaining cognitively intact despite presence of AD neuropathology. Understanding the involved mechanism(s) would lead to development of novel effective therapeutic strategies aimed at promoting synaptic resilience to amyloid toxicity. NDAN have a unique hippocampal post-synaptic proteome when compared with AD and control individuals. Potential upstream modulators of such unique proteomic profile are miRNA-485, miRNA-4723 and miRNA-149, which we found differentially expressed in AD and NDAN vs. control. We thus hypothesized that these miRNAs play an important role in promoting either synaptic resistance or sensitization to Aβ oligomer binding. Using an in vivo mouse model, we found that administration of these miRNAs affected key synaptic genes and significantly decreased Aβ binding to the synapses. Our findings suggest that miRNA regulation and homeostasis are crucial for Aβ interaction with synaptic terminals and support that a unique miRNA regulation could be driving synaptic resistance to Aβ toxicity in NDAN, thus contributing to their preserved cognitive abilities.
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Registered trials
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