ArticleInternational journal of molecular sciences2019
Brain Susceptibility to Methyl Donor Deficiency: From Fetal Programming to Aging Outcome in Rats.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Restoring brain functions in the Mo-blo mouse model of Menkes disease with copper nanoclusters.Science advances · 2026Article
- SIRT1 mediates brain metabolic and developmental consequences of methionine synthase deficiency in inborn errors of cobalamin metabolism.Cell reports. Medicine · 2026Article
- Folate and Cobalamin Deficiencies during Pregnancy Disrupt the Glucocorticoid Response in Hypothalamus throughInternational journal of molecular sciences · 2023Article
- Article
- Interrelation between homocysteine metabolism and the development of autism spectrum disorder in children.Frontiers in molecular neuroscience · 2022Article
- Article
- Epigenetics of the developing and aging brain: Mechanisms that regulate onset and outcomes of brain reorganization.Neuroscience and biobehavioral reviews · 2021Review
- The Stimulation of Neurogenesis Improves the Cognitive Status of Aging Rats Subjected to Gestational and Perinatal Deficiency of B9-12 Vitamins.International journal of molecular sciences · 2020Article
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Abstract
Deficiencies in methyl donors, folate, and vitamin B12 are known to lead to brain function defects. Fetal development is the most studied but data are also available for such an impact in elderly rats. To compare the functional consequences of nutritional deficiency in young versus adult rats, we monitored behavioral outcomes of cerebellum and hippocampus circuits in the offspring of deficient mother rats and in adult rats fed a deficient diet from 2 to 8 months-of-age. We present data showing that the main deleterious consequences are found in young ages compared to adult ones, in terms of movement coordination and learning abilities. Moreover, we obtained sex and age differences in the deleterious effects on these functions and on neuronal layer integrity in growing young rats, while deficient adults presented only slight functional alterations without tissue damage. Actually, the cerebellum and the hippocampus develop and maturate according to different time lap windows and we demonstrate that a switch to a normal diet can only rescue circuits that present a long permissive window of time, such as the cerebellum, whereas the hippocampus does not. Thus, we argue, as others have, for supplements or fortifications given over a longer time than the developmental period.
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