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Now, an international team of scientists has identified a previously unrecognized way to protect the brain from this degeneration. Their research shows that increasing levels of the naturally occurring molecule NAD⁺ can counteract neurological damage linked to Alzheimer’s disease.
Previous research has suggested that boosting NAD⁺ using precursor compounds such as nicotinamide riboside (NR) or nicotinamide mononucleotide (NMN) can produce beneficial effects in animal models of AD and in early-stage clinical studies. However, the biological processes responsible for these effects have remained poorly understood,” explains first author Alice Ruixue Ai.
The new study reveals that NAD⁺ works through a previously unidentified RNA-splicing pathway. This pathway is regulated by a protein called EVA1C, which plays an essential role in the process of RNA splicing. RNA splicing allows a single gene to produce multiple isoforms of a protein, and one isoform may show distinctive effects on the other isoforms. Its dysregulation is one of the most recently acknowledged risk factors for AD.
By Progressive Radio Network4.6
462462 ratings
Now, an international team of scientists has identified a previously unrecognized way to protect the brain from this degeneration. Their research shows that increasing levels of the naturally occurring molecule NAD⁺ can counteract neurological damage linked to Alzheimer’s disease.
Previous research has suggested that boosting NAD⁺ using precursor compounds such as nicotinamide riboside (NR) or nicotinamide mononucleotide (NMN) can produce beneficial effects in animal models of AD and in early-stage clinical studies. However, the biological processes responsible for these effects have remained poorly understood,” explains first author Alice Ruixue Ai.
The new study reveals that NAD⁺ works through a previously unidentified RNA-splicing pathway. This pathway is regulated by a protein called EVA1C, which plays an essential role in the process of RNA splicing. RNA splicing allows a single gene to produce multiple isoforms of a protein, and one isoform may show distinctive effects on the other isoforms. Its dysregulation is one of the most recently acknowledged risk factors for AD.

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