ReviewFrontiers in aging neuroscience2018
U1 snRNP Alteration and Neuronal Cell Cycle Reentry in Alzheimer Disease.
Review in Frontiers in aging neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Multiple Regulatory Mechanisms of Post-Translational Modifications and Therapeutic Potential of Mitotic Catastrophe.International journal of molecular sciences · 2026Review
- Alternative cleavage and polyadenylation: key regulatory mechanisms in health and disease.RNA biology · 2025Review
- Effects of APT20TTMG, a modulator of the U1 snRNP complex, in glioblastoma models.Medical oncology (Northwood, London, England) · 2025Article
- Effects of the therapeutic correction of U1 snRNP complex on Alzheimer's disease.Scientific reports · 2024Article
- Identification of novel genetic loci related to dromedary camel (Camelus dromedarius) morphometrics, biomechanics, and behavior by genome-wide association studies.BMC veterinary research · 2024Article
- U1 snRNA interactions with deep intronic sequences regulate splicing of multiple exons of spinal muscular atrophy genes.Frontiers in neuroscience · 2024Article
- Genome-Wide Mapping Implicates 5-Hydroxymethylcytosines in Diabetes Mellitus and Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023Article
- U1 snRNP proteins promote proximal alternative polyadenylation sites by directly interacting with 3' end processing core factors.Journal of molecular cell biology · 2022Article
- Autophagy regulation by RNA alternative splicing and implications in human diseases.Nature communications · 2022Review
- Advances in Genetics and Epigenetic Alterations in Alzheimer's Disease: A Notion for Therapeutic Treatment.Genes · 2021Review
- Alternative splicing in Alzheimer's disease.Aging clinical and experimental research · 2021Review
- Effects of U1 Small Nuclear Ribonucleoprotein Inhibition on the Expression of Genes Involved in Alzheimer's Disease.ACS omega · 2020Article
- The Critical Role of Nurr1 as a Mediator and Therapeutic Target in Alzheimer's Disease-related Pathogenesis.Aging and disease · 2020Review
- Suboptimal RNA-RNA interaction limits U1 snRNP inhibition of canonical mRNA 3' processing.RNA biology · 2019Article
- U1 snRNA over-expression affects neural oscillations and short-term memory deficits in mice.Cognitive neurodynamics · 2019Article
- The Post-amyloid Era in Alzheimer's Disease: Trust Your Gut Feeling.Frontiers in aging neuroscience · 2019Review
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aberrancy of U1 small nuclear ribonucleoprotein (snRNP) complex and RNA splicing has been demonstrated in Alzheimer's disease (AD). Importantly, the U1 proteopathy is AD-specific, widespread and early-occurring, thus providing a very unique clue to the AD pathogenesis. The prominent feature of U1 histopathology is its nuclear depletion and redistribution in the neuronal cytoplasm. According to the preliminary data, the initial U1 cytoplasmic distribution pattern is similar to the subcellular translocation of the spliceosome in cells undergoing mitosis. This implies that the U1 mislocalization might reflect the neuronal cell cycle-reentry (CCR) which has been extensively evidenced in AD brains. The CCR phenomenon explains the major molecular and cellular events in AD brains, such as Tau and amyloid precursor protein (APP) phosphorylation, and the possible neuronal death through mitotic catastrophe (MC). Furthermore, the CCR might be mechanistically linked to inflammation, a critical factor in the AD etiology according to the genetic evidence. Therefore, the discovery of U1 aberrancy might strengthen the involvement of CCR in the AD neuronal degeneration.
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