ArticleScientific reports2025
Protective role of Karanjin against bisphenol A-Induced cognitive deficits and oxidative damage in a zebrafish model.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
- The Possible Association Between Bisphenol A (BPA) and the Neuropathological Processes Characteristic of Alzheimer's Disease-A Systematic Review of the Literature.International journal of molecular sciences · 2026Pooled it
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bisphenol A (BPA), a persistent environmental contaminant with endocrine-disrupting properties, has been extensively linked to neurotoxicity, leading to cognitive decline, synaptic dysfunction, and neuronal degeneration. It crosses the blood-brain barrier and induces oxidative stress, mitochondrial impairment, and neuroinflammation, leading to neurodegenerative diseases such as Alzheimer's disease. This study investigates the neuroprotective effects of karanjin, a naturally occurring furanoflavonoid, against BPA-induced neurotoxicity using zebrafish (Danio rerio) as a model organism. Adult zebrafish were exposed to 4 mg/L BPA for 21 days, followed by karanjin supplementation at 5 mg/L and 10 mg/L. Standard neuroprotective agents, donepezil and mentat, were used for comparison. Behavioral assessments, including novel tank diving, T-maze, novel object recognition, and Y-maze tests, showed that BPA exposure caused significant impairments in exploratory behavior, learning, and memory, which were reversed by high-dose karanjin. Biochemical analysis indicated BPA exposure elevated acetylcholinesterase (AChE) activity, which was significantly reduced by karanjin. Furthermore, karanjin restored glutathione (GSH) levels, increased superoxide dismutase (SOD) activity, and reduced lipid peroxidation (LPO), indicating strong antioxidant capacity. Histopathological evaluation confirmed karanjin's neuroprotective effects by preserving neuronal integrity and preventing degeneration. These findings suggest karanjin exhibits neuroprotective potential comparable to FDA-approved drugs, warranting further research for therapeutic applications in neurodegenerative disorders.
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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 Socratic graph.