ArticleNeurotoxicity research2020
Maternal Hyperhomocysteinemia Induces Neuroinflammation and Neuronal Death in the Rat Offspring Cortex.
Article in Neurotoxicity research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 28 citations in OpenAlex.
- High-dose folic acid therapy ameliorates gut microbiota dysbiosis in reproductive-aged women with hyperhomocysteinemia.Frontiers in nutrition · 2026Article
- The Role of Purinergic Mechanisms in the Excitability of Trigeminal Afferents of Rats with Prenatal Hyperhomocysteinemia.Biomolecules · 2025Article
- Prenatal Hyperhomocysteinemia Leads to Synaptic Dysfunction and Structural Alterations in the CA1 Hippocampus of Rats.Biomolecules · 2025Article
- Reference Gene Validation in the Embryonic and Postnatal Brain in the Rat Hyperhomocysteinemia Model.Neurotoxicity research · 2024Article
- Diet-induced hyperhomocysteinemia causes sex-dependent deficiencies in offspring musculature and brain function.Frontiers in cell and developmental biology · 2024Article
- Defective quality control autophagy in Hyperhomocysteinemia promotes ER stress and consequent neuronal apoptosis through proteotoxicity.Cell communication and signaling : CCS · 2023Article
- Influence of Immune System Abnormalities Caused by Maternal Immune Activation in the Postnatal Period.Cells · 2023Review
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- Molecular Mechanisms of Cognitive Impairment and Intellectual Disability-Virtual ESN Mini-Conference in Conjunction with the FENS Forum, July 11-15, 2020.Journal of molecular neuroscience : MN · 2020Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Maternal hyperhomocysteinemia is one of the common complications of pregnancy that causes offspring cognitive deficits during postnatal development. In the present work, we evaluated the effect of prenatal hyperhomocysteinemia on structural and ultrastructural organization, neuronal and glial cell number, apoptosis (caspase-3 content and activity), inflammatory markers (tumor necrosis factor-α, interleukin-6, and interleukin-1β), and p38 mitogen-activated protein kinase (p38 MAPK) phosphorylation in the offspring brain cortex in early ontogenesis. Wistar female rats received methionine (0.6 g/kg body weight) by oral administration during pregnancy. Histological and biochemical analyses of 5- and 20-day-old pups' cortical tissue were performed. Lysosome accumulation and other neurodegenerative changes in neurons of animals with impaired embryonic development were investigated by electron microscopy. Neuronal staining (anti-NeuN) revealed a reduction in neuronal number, accompanied by increasing of caspase-3 active form protein level and activity. Maternal hyperhomocysteinemia also elevated the number of astroglial and microglial cells and increased expression of interleukin-1β and p38 MAPK phosphorylation, which indicates the development of neuroinflammatory processes.
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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 OpenQuestion graph.