ArticleMetabolic brain disease2021
Folic acid prevents habituation memory impairment and oxidative stress in an aging model induced by D-galactose.
Article in Metabolic brain disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 19 citations in OpenAlex.
- Deregulation of Neuroinflammatory and Neurotrophic Factors as Biological Events Triggered by D-Galactose Chronic Administration in Wistar Rats.Neuromolecular medicine · 2025Article
- An Update on Neuroaging on Earth and in Spaceflight.International journal of molecular sciences · 2025Review
- Antioxidant and anti-aging role of silk sericin in D-galactose induced mice model.Saudi journal of biological sciences · 2023Article
- Naringin Prevents Cognitive Dysfunction in Aging Rats by Inhibiting Toll-Like Receptor 4 (TLR4)/NF-Evidence-based complementary and alternative medicine : eCAM · 2023Article
- Circ-Vps41 positively modulates Syp and its overexpression improves memory ability in aging mice.Frontiers in molecular neuroscience · 2022Article
- Oral administration of D-galactose increases brain tricarboxylic acid cycle enzymes activities in Wistar rats.Metabolic brain disease · 2021Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to evaluate the effect of folic acid treatment in an animal model of aging induced by D-galactose (D-gal). For this propose, adult male Wistar rats received D-gal intraperitoneally (100 mg/kg) and/or folic acid orally (5 mg/kg, 10 mg/kg or 50 mg/kg) for 8 weeks. D-gal caused habituation memory impairment, and folic acid (10 mg/kg and 50 mg/kg) reversed this effect. However, folic acid 50 mg/kg per se caused habituation memory impairment. D-gal increased the lipid peroxidation and oxidative damage to proteins in the prefrontal cortex and hippocampus from rats. Folic acid (5 mg/kg, 10 mg/kg, or 50 mg/kg) partially reversed the oxidative damage to lipids in the hippocampus, but not in the prefrontal cortex, and reversed protein oxidative damage in the prefrontal cortex and hippocampus. D-gal induced synaptophysin and BCL-2 decrease in the hippocampus and phosphorylated tau increase in the prefrontal cortex. Folic acid was able to reverse these D-gal-related alterations in the protein content. The present study shows folic acid supplementation as an alternative during the aging to prevent cognitive impairment and brain alterations that can cause neurodegenerative diseases. However, additional studies are necessary to elucidate the effect of folic acid in aging.
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