ArticleIBRO neuroscience reports2026
Article in IBRO neuroscience reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Olfactory dysfunction is a debilitating yet under-investigated sequela of ischemic stroke, for which no approved pharmacological intervention currently exists. Despite the documented ethnomedicinal use of Purpose: To establish a reproducible rat model of post-stroke olfactory dysfunction and evaluate the neuroprotective effects of an aqueous extract of Methods: A modified transient global cerebral ischemia-reperfusion model was developed in male Wistar rats via bilateral common and internal carotid artery occlusion. Animals were treated with AELC (140, 280, and 560 mg/kg), minocycline (100 mg/kg), or piracetam (250 mg/kg) as reference compounds. Evaluations encompassed neurological recovery, thermoregulatory profiling, olfacto-cognitive behavioral testing, and biochemical and histological analyses of the olfactory bulb, piriform cortex, prefrontal cortex, and hippocampus. Mechanistic insights were sought through LC-MS phytochemical profiling, Results: Ischemia-reperfusion induced severe thermoregulatory failure, locomotor deficits, and significant olfactory dysfunction (Hedges' g > 2.00), correlating with acetylcholine depletion, oxidative stress (elevated MDA and nitrites; depleted GSH), and neuroinflammation (elevated IL-1β and TNF-α). Histological examination confirmed significant neuronal pyknosis, ghost cell formation, and architectural disorganization across the olfacto-mnemonic axis. AELC at 280 and 560 mg/kg effectively reversed these deficits, restoring cholinergic tone (p < 0.001) and preserving neuronal microarchitecture comparably to reference compounds. LC-MS and Conclusion: These findings establish a reliable rat model of post-stroke olfactory dysfunction and demonstrate that
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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 Socratic graph.