ArticleScientific reports2023
Necrosulfonamide exerts neuroprotective effect by inhibiting necroptosis, neuroinflammation, and α-synuclein oligomerization in a subacute MPTP mouse model of Parkinson's disease.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 30 citations in OpenAlex.
- Integrated Necroptosis Within Programmed Cell Death in Traumatic Brain Injury.Molecular neurobiology · 2026Review
- Targeting non-apoptotic regulated cell death (RCD) to treat neurodegenerative diseases.Acta pharmaceutica Sinica. B · 2026Review
- Non-canonical cell death in neurodegeneration: emerging mechanisms and therapeutic Frontiers.Apoptosis : an international journal on programmed cell death · 2026Review
- Enhanced therapeutic potential of paeoniflorin and vitamin B12 in intracerebropeduncle ethidium bromide-induced multiple sclerosis-like pathology.Frontiers in pharmacology · 2026Article
- Cannabidiol-Induced Tumor Cell Death: Molecular Mechanisms and Translational Perspectives in Cancer Therapy.Drug design, development and therapy · 2026Review
- Design, Spectral Insights, and Enhanced Antioxidant Potential of Novel Phenothiazine DerivativesAnti-inflammatory & anti-allergy agents in medicinal chemistry · 2026Article
- Cystatin F as a neuroimmune effector in CNS inflammation and neurodegeneration.Frontiers in cell and developmental biology · 2026Review
- Gasdermins in neurodegeneration: emerging mechanisms and therapeutic targets.Cell death & disease · 2025Review
- ZLN005 Alleviates the Dopaminergic Degeneration via PGC-1α-Mediated Mitochondrial Homeostasis in Parkinson's Disease.Molecular neurobiology · 2025Article
- TNF as a mediator of metabolic inflammation and body-brain interaction in obesity-driven neuroinflammation and neurodegeneration.Ageing research reviews · 2025Review
- Mixed Lineage Kinase Domain-Like Protein (MLKL): From Mechanisms to Therapeutic Opportunities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Cystatin F-a key player in central nervous system disease.Journal of neuroinflammation · 2025Review
- Sulphonylureas as Adjunct Therapeutic Agents in the Treatment of Autoimmune Conditions: A Narrative Review.Pharmacology research & perspectives · 2025Review
- Templating of monomeric alpha-synuclein results in inflammation and SNpc dopamine neuron death in a genetic mouse model of induced synucleinopathy.Scientific reports · 2025Article
- New Insights on the Potential Role of Pyroptosis in Parkinson's Neuropathology and Therapeutic Targeting of NLRP3 Inflammasome with Recent Advances in Nanoparticle-Based miRNA Therapeutics.Molecular neurobiology · 2025Review
- PRV Induces Neurological Inflammatory Injury by Activating Necroptosis of Brain Tissue.Microorganisms · 2025Article
- MLKL Inhibitor Reduces Oxidative Stress, Inflammation, and Dopaminergic Neuronal Cell Death in MPTP-Induced Parkinson's Disease Mouse Model.Biomolecules & therapeutics · 2025Article
- The interplay of iron, oxidative stress, and α-synuclein in Parkinson's disease progression.Molecular medicine (Cambridge, Mass.) · 2025Review
- NLRP3 inflammasome in neuroinflammation and central nervous system diseases.Cellular & molecular immunology · 2025Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is an incurable movement disorder characterized by dopaminergic cell loss, neuroinflammation, and α-synuclein pathology. Herein, we investigated the therapeutic effects of necrosulfonamide (NSA), a specific inhibitor of mixed lineage kinase domain-like protein (MLKL), in a subacute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. MLKL is an executor of necroptosis, a programmed cell death pathway that causes inflammation. Repeated administration of NSA resulted in the recovery of impaired motor performance and dopaminergic degeneration. Furthermore, NSA inhibited the phosphorylation, ubiquitylation, and oligomerization of MLKL, all of which are associated with MLKL cell death-inducing activity in dopaminergic cells in the substantia nigra (SN). NSA also inhibited microglial activation and reactive astrogliosis as well as the MPTP-induced expression of proinflammatory molecules such as tumor necrosis factor-α, interleukin-1β, inducible nitric oxide synthase, and cystatin F. Furthermore, NSA inhibited α-synuclein oligomerization and phosphorylation in the SN of MPTP-treated mice by inhibiting the activity of glycogen synthase kinase 3β and matrix metalloproteinase-3. In conclusion, NSA has anti-necroptotic, anti-inflammatory, and anti-synucleinopathic effects on PD pathology. Therefore, NSA is a potential therapeutic candidate for PD.
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