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• W3087078276 abstract "Alzheimer’s disease (AD) is a progressively debilitating neurodegenerative disorder that has no effective remedy, so far, with available therapeutic modalities being only symptomatic and of modest efficacy. Necroptosis is a form of controlled cell death with a recently emerging link to the pathogenesis of several neurodegenerative diseases. This study investigated the role of necroptosis in the pathogenesis of AD and evaluated the potential beneficial effect of the necroptosis inhibitor, necrosulfonamide (NSA), in a rat model of AD. AD was induced by oral administration of AlCl3 (17 mg/kg/day) for 6 consecutive weeks. Administration of NSA (1.65 mg/kg/day) intraperitoneally for 6 weeks significantly amended AlCl3-induced spatial learning and memory deficits, as demonstrated by enhanced rat performance in Morris water and Y-mazes. NSA alleviated the abnormally high hippocampal expression of tumor necrosis factor-alpha (TNF-α), β-site amyloid precursor protein cleaving enzyme 1 (BACE1), β-amyloid, glycogen synthase kinase-3β (GSK-3β), phosphorylated tau protein, and acetylcholinesterase with concordant replenishment of acetylcholine. The amendments of AD perturbations achieved by NSA correlated with its inhibitory effect on the phosphorylation of the key necroptotic executioner, mixed lineage kinase domain-like protein (MLKL). Histopathological alterations supported the biochemical findings. In conclusion, NSA treatment represents a promising anti-Alzheimer’s approach, mitigating AD neuropathologies via targeting MLKL-dependent necroptosis." @default.
• W3087078276 created "2020-09-25" @default.
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• W3087078276 date "2020-09-16" @default.
• W3087078276 modified "2023-10-17" @default.
• W3087078276 title "Ameliorative Effect of Necrosulfonamide in a Rat Model of Alzheimer’s Disease: Targeting Mixed Lineage Kinase Domain-like Protein-Mediated Necroptosis" @default.
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• W3087078276 doi "https://doi.org/10.1021/acschemneuro.0c00516" @default.
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