ArticleAging cell2018
Spontaneous development of Alzheimer's disease-associated brain pathology in a Shugoshin-1 mouse cohesinopathy model.
Article in Aging cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Development of Animal Models for Preclinical Testing of hPSCs Products.Advances in experimental medicine and biology · 2025Review
- Haploinsufficiency and Alzheimer's Disease: The Possible Pathogenic and Protective Genetic Factors.International journal of molecular sciences · 2024Review
- Mechanisms and Functions of Activity-Regulated Cytoskeleton-Associated Protein in Synaptic Plasticity.Molecular neurobiology · 2023Review
- A role for Shugoshin in human cilia?microPublication biology · 2023Article
- R-loop Mediated DNA Damage and Impaired DNA Repair in Spinal Muscular Atrophy.Frontiers in cellular neuroscience · 2022Review
- Powerful gene-based testing by integrating long-range chromatin interactions and knockoff genotypes.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- How would preclinical Alzheimer's disease (AD pathology) occur? An insight from a genomic instability mouse model.Neural regeneration research · 2021Article
- Cohesin-protein Shugoshin-1 controls cardiac automaticity via HCN4 pacemaker channel.Nature communications · 2021Article
- GNG13 Is a Potential Marker of the State of Health of Alzheimer's Disease Patients' Cerebellum.Journal of molecular neuroscience : MN · 2021Article
- GSK3-ARC/Arg3.1 and GSK3-Wnt signaling axes trigger amyloid-β accumulation and neuroinflammation in middle-aged Shugoshin 1 mice.Aging cell · 2020Article
- Functioning mechanisms of Shugoshin-1 in centromeric cohesion during mitosis.Essays in biochemistry · 2020Review
- "Amyloid-beta accumulation cycle" as a prevention and/or therapy target for Alzheimer's disease.Aging cell · 2020Review
- The expanding phenotypes of cohesinopathies: one ring to rule them all!Cell cycle (Georgetown, Tex.) · 2019Review
- The X Files: "The Mystery of X Chromosome Instability in Alzheimer's Disease".Frontiers in genetics · 2019Review
- Chromosome Instability and Mosaic Aneuploidy in Neurodegenerative and Neurodevelopmental Disorders.Frontiers in genetics · 2019Article
- Spontaneous development of Alzheimer's disease-associated brain pathology in a Shugoshin-1 mouse cohesinopathy model.Aging cell · 2018Article
- Critical role of mitosis in spontaneous late-onset Alzheimer's disease; from a Shugoshin 1 cohesinopathy mouse model.Cell cycle (Georgetown, Tex.) · 2018Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Spontaneous late-onset Alzheimer's disease (LOAD) accounts for more than 95% of all human AD. As mice do not normally develop AD and as understanding on molecular processes leading to spontaneous LOAD has been insufficient to successfully model LOAD in mouse, no mouse model for LOAD has been available. Existing mouse AD models are all early-onset AD (EOAD) models that rely on forcible expression of AD-associated protein(s), which may not recapitulate prerequisites for spontaneous LOAD. This limitation in AD modeling may contribute to the high failure rate of AD drugs in clinical trials. In this study, we hypothesized that genomic instability facilitates development of LOAD and tested two genomic instability mice models in the brain pathology at the old age. Shugoshin-1 (Sgo1) haploinsufficient (∓) mice, a model of chromosome instability (CIN) with chromosomal and centrosomal cohesinopathy, spontaneously exhibited a major feature of AD pathology; amyloid beta accumulation that colocalized with phosphorylated Tau, beta-secretase 1 (BACE), and mitotic marker phospho-Histone H3 (p-H3) in the brain. Another CIN model, spindle checkpoint-defective BubR1
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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.