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As an alternative methyl donor, betaine plays a central role in maintaining methylation capacity, and its depletion may contribute to elevations in S-adenosylhomocysteine and impaired methyltransferase activity

As previously described, common molecular contributors to neurodegeneration such as oxidative stress, mitochondrial dysfunction, and glial activation also play central roles in MS pathogenesis

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We reported for the first time that PRMT1 knockdown restored fatty acid metabolism in TECs, thus improving energy homeostasis and reducing lipid accumulation and kidney injury