ArticleScientific reports2019
Heterochromatic genome instability and neurodegeneration sharing similarities with Alzheimer's disease in old Bmi1+/- mice.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 42 citations in OpenAlex.
- Phosphorylated ubiquitin is a secondary messenger and an epigenetic mark mediating mitochondria to nucleus signaling.bioRxiv : the preprint server for biology · 2026Article
- BMI1 represses G-quadruplex DNA formation to maintain genomic stability during replication.The Journal of biological chemistry · 2026Article
- Modeling Late-Onset Sporadic Alzheimer's Disease Using Patient-Derived Cells: A Review.Neurology international · 2026Review
- Comprehensive profiling of L1 retrotransposons in mouse.Nucleic acids research · 2024Article
- Biomarker profiling to determine clinical impact of microRNAs in cognitive disorders.Scientific reports · 2024Article
- Transposable Elements: Emerging Therapeutic Targets in Neurodegenerative Diseases.Neurotoxicity research · 2024Review
- Tau mediates the reshaping of the transcriptional landscape toward intermediate Alzheimer's disease stages.Frontiers in cell and developmental biology · 2024Article
- Histone post-translational modification and heterochromatin alterations in neurodegeneration: revealing novel disease pathways and potential therapeutics.Frontiers in molecular neuroscience · 2024Review
- Repetitive elements in aging and neurodegeneration.Trends in genetics : TIG · 2023Review
- Megakaryopoiesis impairment through acute innate immune signaling activation by azacitidine.The Journal of experimental medicine · 2022Article
- Histone H2A ubiquitination resulting from Brap loss of function connects multiple aging hallmarks and accelerates neurodegeneration.iScience · 2022Article
- The Complex Mechanisms by Which Neurons Die Following DNA Damage in Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- The relevance of polycomb group proteins to the development of psychiatric disorders.Frontiers in cell and developmental biology · 2022Article
- Alzheimer's disease: a tale of two diseases?Neural regeneration research · 2021Review
- Nuclear dynamics and stress responses in Alzheimer's disease.Molecular neurodegeneration · 2021Review
- Perturbed DNA methylation by Gadd45b induces chromatin disorganization, DNA strand breaks and dopaminergic neuron death.iScience · 2021Article
- Review
- G-quadruplexes originating from evolutionary conserved L1 elements interfere with neuronal gene expression in Alzheimer's disease.Nature communications · 2021Article
- Review
- Epigenome signatures landscaped by histone H3K9me3 are associated with the synaptic dysfunction in Alzheimer's disease.Aging cell · 2020Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Sporadic Alzheimer's disease (AD) is the most common cause of dementia. However, representative experimental models of AD have remained difficult to produce because of the disease's uncertain origin. The Polycomb group protein BMI1 regulates chromatin compaction and gene silencing. BMI1 expression is abundant in adult brain neurons but down-regulated in AD brains. We show here that mice lacking one allele of Bmi1 (Bmi1+/-) develop normally but present with age cognitive deficits and neurodegeneration sharing similarities with AD. Bmi1+/- mice also transgenic for the amyloid beta precursor protein died prematurely and present aggravated disease. Loss of heterochromatin and DNA damage response (DDR) at repetitive DNA sequences were predominant in Bmi1+/- mouse neurons and inhibition of the DDR mitigated the amyloid and Tau phenotype. Heterochromatin anomalies and DDR at repetitive DNA sequences were also found in AD brains. Aging Bmi1+/- mice may thus represent an interesting model to identify and study novel pathogenic mechanisms related to AD.
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Registered trials
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