ArticleMetabolic brain disease2022
Adenosine protects D-galactose induced alterations in rat model of aging via attenuating neurochemical profile and redox status.
Article in Metabolic brain disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 2 papers.
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.
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Article
- Mitigation of behavioral deficits and cognitive impairment by antioxidant and neuromodulatory potential ofSaudi journal of biological sciences · 2023Article
Corrections and comments
- Retracted
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is the process that every organism faces. The aging model of brain has been developed by the use of d-galactose (d-Gal). Adenosine (Ad) being a neuroprotective agent that has been utilized in treatment of various neurological disorders. The aim of current study is to evaluate the outcome of Ad on d-Gal induced neurotoxicity which caused behavioral deficits, memory impairment and oxidative stress. Rats were treated with d-Gal at a dose of 300 mg/ml/kg and Ad 1 mg/ml/kg; intraperitoneally for 28 days. Behavioral assessment was performed after the treatment period. Animals were sacrificed after behavioral tests and their brains were collected, hippocampus were removed for biochemical and neurochemical analysis. The results showed that administration of Ad ameliorates the negative effects of d-Gal induced aging in various behavioral tests and increased the time spent in the open arm and light box in elevated plus maze (EPM) and light dark activity (LDA) tests respectively indicate anxiolytic effect; increased the mobility time in tail suspension test (TST) shows antidepressant effect; decreased escape latencies in Morris water maze (MWM) acquisition trials, increase entries and time spent in the target quadrant suggests improvement in learning ability of animals. Administration of Ad also decreased malondialdehyde (MDA) levels, increased antioxidant enzymes activity; decreased acetylcholinesterase (AChE) activity, increased 5-hydroxytryptamine (5-HT, serotonin) metabolism and normalized histopathological alteration in the hippocampus. It is concluded that anxiety, depression and memory impairment induced by d-Gal were protected by Ad through its antioxidant and neuro-modulatory effects.
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Registered trials
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