Vitamin B
| Autor: | Andy B, Lam, Kirsten, Kervin, Jessica E, Tanis |
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| Rok vydání: | 2021 |
| Předmět: | |
| Zdroj: | Cell reports |
| ISSN: | 2211-1247 |
| Popis: | SUMMARY Alzheimer’s disease (AD) is a devastating neurodegenerative disorder with no effective treatment. Diet, as a modifiable risk factor for AD, could potentially be targeted to slow disease onset and progression. However, complexity of the human diet and indirect effects of the microbiome make it challenging to identify protective nutrients. Multiple factors contribute to AD pathogenesis, including amyloid beta (Aβ) deposition, energy crisis, and oxidative stress. Here, we use Caenorhabditis elegans to define the impact of diet on Aβ proteotoxicity. We discover that dietary vitamin B12 alleviates mitochondrial fragmentation, bioenergetic defects, and oxidative stress, delaying Aβ-induced paralysis without affecting Aβ accumulation. Vitamin B12 has this protective effect by acting as a cofactor for methionine synthase, impacting the methionine/S-adenosylmethionine (SAMe) cycle. Vitamin B12 supplementation of B12-deficient adult Aβ animals is beneficial, demonstrating potential for vitamin B12 as a therapy to target pathogenic features of AD triggered by proteotoxic stress. Graphical Abstract In brief Lam et al. discover that feeding a vitamin-B12-deficient diet to amyloid beta (Aβ)-expressing C. elegans accelerates paralysis, reduces ATP levels, and increases oxidative stress. Their results indicate that vitamin B12 affects the methionine/SAMe cycle to protect against Aβ-induced proteotoxicity. |
| Databáze: | OpenAIRE |
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