ArticleAging2019
Brain-specific NRSF deficiency aggravates dopaminergic neurodegeneration and impairs neurogenesis in the MPTP mouse model of Parkinson's disease.
Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- DYRK1A and Parkinson's disease, facts and hypotheses.Neurobiology of disease · 2026Review
- Tamoxifen attenuates manganese-induced dysregulation of neuronal REST via the genomic ER-Frontiers in molecular neuroscience · 2025Article
- Revisiting the role of cancer-associated fibroblasts in tumor microenvironment.Frontiers in immunology · 2025Review
- REST Is Not Resting: REST/NRSF in Health and Disease.Biomolecules · 2023Review
- REST in the Road Map of Brain Development.Cellular and molecular neurobiology · 2023Review
- Evaluation of the therapeutic potential of cerebrolysin and/or lithium in the male Wistar rat model of Parkinson's disease induced by reserpine.Metabolic brain disease · 2023Article
- Systematic analysis identifies REST as an oncogenic and immunological biomarker in glioma.Scientific reports · 2023Article
- Article
- Brain-Region Specific Metabolic Abnormalities in Parkinson's Disease and Levodopa-Induced Dyskinesia.Frontiers in aging neuroscience · 2020Article
- Review
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Degeneration of the dopaminergic neurons in the substantia nigra and the resultant dopamine depletion from the striatum are the hallmarks of Parkinson's disease (PD) and are responsible for the disease's cardinal motor symptoms. The transcriptional repressor Neuron-Restrictive Silencer Factor (NRSF), also known as RE1-Silencing Transcription Factor (REST), was originally identified as a negative regulator of neuron-specific genes in non-neuronal cells. Our previous study showed that mice deficient in neuronal NRSF/REST expression were more vulnerable to the noxious effects of the dopaminergic neurotoxin MPTP. Here, we found that brain-specific deletion of
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