ArticleActa neuropathologica communications2018
Formation of Toxic Oligomeric Assemblies of RNA-binding Protein: Musashi in Alzheimer's disease.
Article in Acta neuropathologica communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Pooled it
- Hippocampal neural stem cell-derived extracellular vesicles modulate microglia to promote resilience against tau oligomers.Neural regeneration research · 2026Article
- Article
- ELAVL1 and ELAVL4 are required for Musashi-dependent translational activation.bioRxiv : the preprint server for biology · 2026Article
- Nuclear dysfunction in aging and neurodegeneration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Riboregulation: a non-canonical tau function.Molecular neurodegeneration · 2026Review
- MSI1 Accelerates Prostate Cancer Cell Proliferation, Migration and Glycolysis by Promoting ABHD2 Transcription.Biochemical genetics · 2026Article
- Dysregulated mRNA Translation in Alzheimer's Disease: Mechanisms, Therapeutic Opportunities, and Challenges for Clinical Translation.Clinical interventions in aging · 2026Review
- Human Wild-Type α-Synuclein Drives Progressive Tau Pathology in a Disease-Relevant Mouse Model of Synucleinopathy.Research square · 2025Article
- Hippocampal Neural Stem Cell Exosomes Promote Brain Resilience against the Impact of Tau Oligomers.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Pathogenic oligomeric Tau alters neuronal RNA processes through the formation of nuclear heteromeric amyloids with RNA-binding protein Musashi1.Progress in neurobiology · 2025Article
- A Holistic Analysis of Alzheimer's Disease-Associated lncRNA Communities Reveals Enhanced lncRNA-miRNA-RBP Regulatory Triad Formation Within Functionally Segregated Clusters.Journal of molecular neuroscience : MN · 2024Article
- Tau-RNA complexes inhibit microtubule polymerization and drive disease-relevant conformation change.Brain : a journal of neurology · 2023Article
- Cerebrospinal Fluid Protein Biomarker Discovery in CLN3.Journal of proteome research · 2023Article
- The paralogues MAGOH and MAGOHB are oncogenic factors in high-grade gliomas and safeguard the splicing of cell division and cell cycle genes.RNA biology · 2023Article
- RNA-Binding Proteins as Epigenetic Regulators of Brain Functions and Their Involvement in Neurodegeneration.International journal of molecular sciences · 2022Review
- Tau interactome and RNA binding proteins in neurodegenerative diseases.Molecular neurodegeneration · 2022Review
- Phase separation driven by interchangeable properties in the intrinsically disordered regions of protein paralogs.Communications biology · 2022Article
- Aβ/tau oligomer interplay at human synapses supports shifting therapeutic targets for Alzheimer's disease.Cellular and molecular life sciences : CMLS · 2022Article
- The prion-like transmission of tau oligomersFrontiers in aging neuroscience · 2022Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is the most common neurodegenerative disorder associated with structural and functional alterations of brain cells causing progressive deterioration of memory and other cognitive functions. Recent studies demonstrate that several neurodegenerative diseases, including AD exhibit RNA-binding proteins (RBPs) pathologies, including TAR DNA -binding protein (TDP-43), fused in sarcoma (FUS), superoxide dismutase (SOD1) and T-interacting antigen-1 (TIA-1), highlighting the role of RBPs in neurodegeneration. One such group of RBPs, Musashi proteins comprised of MSI1 and MSI2, has been long studied in neurogenesis and cancer biology. Herein, we have investigated the aggregation properties of MSI1 and MSI2 by in vitro assays, their expression and accumulation as well as their possible interactions with other cellular proteins, such as tau in AD pathology. We have performed atomic force microscopy, Western blot, and immunoprecipitation to demonstrate the aggregation properties of recombinant Musashi proteins. Furthermore, we have studied cortical brain sections from AD (N = 4) and age-matched non-demented subjects (N = 4) by Western blot and immunofluorescence microscopy to investigate MSI1 and MSI2 levels and their localization in human brain tissues. Musashi proteins showed in vitro aggregation properties by forming oligomers. We have observed an increase in Musashi proteins levels in AD brain tissues as compared with age-matched non-demented subjects. Moreover, Musashi proteins are observed to form oligomers in the diseased brain tissues. Interestingly, the co-immunofluorescence study has revealed a change in fluorescence pattern of oligomeric Musashi proteins and tau with a high association in the perinuclear area of the cells suggesting changes in function of Musashi proteins. Our data have demonstrated for the first time that MSI1 and MSI2 are present in an oligomeric state in AD brains compared to the age-matched non-demented subjects and that these large assemblies co-localize with tau contributing to the neurodegenerative pathogenesis.
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Registered trials
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