ArticleJCI insight2024
Neuronal deletion of the circadian clock gene Bmal1 induces cell-autonomous dopaminergic neurodegeneration.
Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- Conditional deletion of Bmal1 modestly alters acute pathology without affecting functional recovery after contusive spinal cord injury.Neuroscience letters · 2026Article
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- The ClockJournal of orthopaedic surgery and research · 2026Article
- Time vortex: the circadian-dopaminergic dialogue in Parkinson's disease.NPJ Parkinson's disease · 2026Review
- The biological clock in parkinson's disease: mechanisms and chronotherapy.NPJ Parkinson's disease · 2026Review
- The astrocyte clock controls circadian perineuronal net remodeling, synapse strength and learning behavior.bioRxiv : the preprint server for biology · 2026Article
- Distinct radial glia subtypes regulate midbrain dopaminergic neuron development.Nature neuroscience · 2026Article
- Circadian disruption as a driver and target in neurodegenerative diseases: from molecular mechanisms to chronotherapeutic strategies.Metabolic brain disease · 2026Review
- Dual roles of circadian clock proteins in development and adult homeostasis.Npj biological timing and sleep · 2026Review
- Core Circadian Protein BMAL1: Implication for Nervous System Functioning and Its Diseases.Brain sciences · 2025Review
- The 4E-BPs as Translational Regulators in Neurological Disorders: Molecular Mechanisms and Therapeutic Potential.Molecular neurobiology · 2025Review
- [ModifiedNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Article
- The intersection of circadian rhythms and the blood-brain barrier with drug efficacy and delivery in neurological disorders.Advanced drug delivery reviews · 2025Review
- Circadian system and aging: where both times interact.Frontiers in aging · 2025Review
- Exploring the interplay between circadian rhythms and prostate cancer: insights into androgen receptor signaling and therapeutic opportunities.Frontiers in cell and developmental biology · 2024Review
- Bmal1 haploinsufficiency impairs fear memory and modulates neuroinflammation via the 5-HT2C receptor.Frontiers in pharmacology · 2024Article
- Saponin components inFrontiers in pharmacology · 2024Review
- Circadian rhythm disruption: a potential trigger in Parkinson's disease pathogenesis.Frontiers in cellular neuroscience · 2024Review
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
Circadian rhythm dysfunction is a hallmark of Parkinson disease (PD), and diminished expression of the core clock gene Bmal1 has been described in patients with PD. BMAL1 is required for core circadian clock function but also serves nonrhythmic functions. Germline Bmal1 deletion can cause brain oxidative stress and synapse loss in mice, and it can exacerbate dopaminergic neurodegeneration in response to the toxin MPTP. Here we examined the effect of cell type-specific Bmal1 deletion on dopaminergic neuron viability in vivo. We observed that global, postnatal deletion of Bmal1 caused spontaneous loss of tyrosine hydroxylase+ (TH+) dopaminergic neurons in the substantia nigra pars compacta (SNpc). This was not replicated by light-induced disruption of behavioral circadian rhythms and was not induced by astrocyte- or microglia-specific Bmal1 deletion. However, either pan-neuronal or TH neuron-specific Bmal1 deletion caused cell-autonomous loss of TH+ neurons in the SNpc. Bmal1 deletion did not change the percentage of TH neuron loss after α-synuclein fibril injection, though Bmal1-KO mice had fewer TH neurons at baseline. Transcriptomics analysis revealed dysregulation of pathways involved in oxidative phosphorylation and Parkinson disease. These findings demonstrate a cell-autonomous role for BMAL1 in regulating dopaminergic neuronal survival and may have important implications for neuroprotection in PD.
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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.