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From the article:

Scientists treated both normal mice and mice with a mutation in the gene responsible for Werner’s syndrome (WRN gene) with vitamin C in drinking water. Before treatment, the mice with a mutated WRN gene were fat, diabetic, and developing heart disease and cancer. After treatment, the mutant mice were as healthy as the normal mice and lived a normal lifespan. Vitamin C also improved how the mice stored and burned fat, decreased tissue inflammation and decreased oxidative stress in the WRN mice.

From actual publication, rather than press release:

Daily ascorbate supplementation allowed [Werner mice] to recover a normal mean life span and healthy aging. Although the number of animals used in each cohort was not big enough for a statistical testing on maximum life span, ascorbate treatment did prevent the appearance of Werner syndrome characteristic redox imbalance and related genomic damage. It also prevented the liver proinflammatory status observed in [Werner mice].

What’s someone unexpected about the fact that additional vitamin C restoring mean lifespan is the fact that Werner syndrome is associated with higher-than-usual ascorbate status rather than reduced, so supplementing with vitamin C being beneficial may be somewhat counter to expectation:

Interestingly, blood ascorbate levels increased with phenotypic progression in [Werner mice]. Ascorbate being protective, it is possible that the retention of vitamin C is a defense mechanism to counterbalance the age‐dependent rise in oxidative stress. We cannot rule out, however, the possibility that the increased ascorbate levels observed in [Werner mice] are due to a modification in ascorbate metabolism only specific to these mice.

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