The effects of folic acid on RNA m6A methylation in hippocampus as well as learning and memory ability of rats with acute lead exposure

Li, Ning; Zhang, Di; Cao, Sheng; Qiao, Mingqiang; Zhang, Pingan; Zhao, Qiuyan; Shen, Yue; Huang, Xianqing; Luo, Song

doi:10.1016/j.jff.2020.104276

Cited by 9 publications

(6 citation statements)

References 38 publications

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“…Previous reports indicated that lead exposure resulted in a decline in learning and memory ability in SD rats, accompanied by a decrease in m 6 A level in the hippocampus. Furthermore, learning memory and m 6 A levels were improved after folic acid intervention [ 81 ]. LPS-induced microglial activation and inflammatory responses were potentially mediated by enhanced m 6 A methylation and stability of Gbp11 and Cp mRNA through IGF2BP1 [ 82 ].…”

Section: Discussionmentioning

confidence: 99%

Betaine alleviates cognitive impairment induced by homocysteine through attenuating NLRP3-mediated microglial pyroptosis in an m6A-YTHDF2-dependent manner

Yang,

Huang,

Zhong

et al. 2024

Redox Biology

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Section: Discussionmentioning

confidence: 99%

Betaine alleviates cognitive impairment induced by homocysteine through attenuating NLRP3-mediated microglial pyroptosis in an m6A-YTHDF2-dependent manner

Yang,

Huang,

Zhong

et al. 2024

Redox Biology

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“…In addition, a small number of studies have explored the effect of environmental exposures on RNA modifications and expression of RNA in brain or in brain-related cell lines. With these new studies, evidence is growing to support that exposure to many types of neurotoxicants (including dioxin, arsenic, lead, atrazine, cobalt, paraquat) affects both expression of RNA modulators and the patterns of RNA modifications in brain and brain-derived cell lines [18,[121][122][123][124][125].…”

Section: Modifications and Environmental Exposuresmentioning

confidence: 99%

Emerging Role of Environmental Epitranscriptomics and RNA Modifications in Parkinson’s Disease

Gionco,

Bernstein

2024

JPD

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Environmental risk factors and gene-environment interactions play a critical role in Parkinson’s disease (PD). However, the relatively large contribution of environmental risk factors in the overwhelming majority of PD cases has been widely neglected in the field. A “PD prevention agenda” proposed in this journal laid out a set of research priorities focused on preventing PD through modification of environmental risk factors. This agenda includes a call for preclinical studies to employ new high-throughput methods for analyzing transcriptomics and epigenomics to provide a deeper understanding of the effects of exposures linked to PD. Here, we focus on epitranscriptomics as a novel area of research with the potential to add to our understanding of the interplay between genes and environmental exposures in PD. Both epigenetics and epitranscriptomics have been recognized as potential mediators of the complex relationship between genes, environment, and disease. Multiple studies have identified epigenetic alterations, such as DNA methylation, associated with PD and PD-related exposures in human studies and preclinical models. In addition, recent technological advancements have made it possible to study epitranscriptomic RNA modifications, such as RNA N6-methyladenosine (m6A), and a handful of recent studies have begun to explore epitranscriptomics in PD-relevant exposure models. Continued exploration of epitranscriptomic mechanisms in environmentally relevant PD models offers the opportunity to identify biomarkers, pre-degenerative changes that precede symptom onset, and potential mitigation strategies for disease prevention and treatment.

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“…Folic acid, a water-soluble B vitamin, reduces the production of Aβ and slows the progression of AD by involving in generating S-adenosylmethionine (SAM), potentially enhancing the levels of RNA m 6 A methylation ( Li et al, 2015 ; Li N. et al, 2021 ), implying that RNA m 6 A methylation may be involved in Aβ metabolism. Interestingly, Aβ treatment was found to have significantly reduced METTL3 and postsynaptic density-95 (PSD-95) expression in rat primary cortical neurons.…”

Section: Rna N6-methyladenosine Methylation In Alzheimer’s Diseasementioning

confidence: 99%

RNA N6-Methyladenosine Modifications and Its Roles in Alzheimer’s Disease

Zhang

Guo

et al. 2022

Front. Cell. Neurosci.

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The importance of epitranscriptomics in regulating gene expression has received widespread attention. Recently, RNA methylation modifications, particularly N6-methyladenosine (m6A), have received marked attention. m6A, the most common and abundant type of eukaryotic methylation modification in RNAs, is a dynamic reversible modification that regulates nuclear splicing, stability, translation, and subcellular localization of RNAs. These processes are involved in the occurrence and development of many diseases. An increasing number of studies have focused on the role of m6A modification in Alzheimer’s disease, which is the most common neurodegenerative disease. This review focuses on the general features, mechanisms, and functions of m6A methylation modification and its role in Alzheimer’s disease.

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The effects of folic acid on RNA m6A methylation in hippocampus as well as learning and memory ability of rats with acute lead exposure

Cited by 9 publications

References 38 publications

Betaine alleviates cognitive impairment induced by homocysteine through attenuating NLRP3-mediated microglial pyroptosis in an m6A-YTHDF2-dependent manner

Betaine alleviates cognitive impairment induced by homocysteine through attenuating NLRP3-mediated microglial pyroptosis in an m6A-YTHDF2-dependent manner

Emerging Role of Environmental Epitranscriptomics and RNA Modifications in Parkinson’s Disease

RNA N6-Methyladenosine Modifications and Its Roles in Alzheimer’s Disease

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