Fight Aging!

Scientists like to conduct studies using mouse lineages that exhibit forms of accelerated aging, as a faster study is a cheaper study. These mice do not exhibit accelerated aging per se, of course. Each lineage suffers from some sort of increased production of cell and tissue damage, leading to a faster onset of conditions akin to natural age-related diseases. Aging itself is a matter of damage accumulation, but it is usually the case that the types and mix of damage matters when it comes to drawing conclusions from an animal study. Not always, though. In today's open access paper, that the mice are damaged in ways that cause a faster onset of age-related disability and disease doesn't detract from the finding that resetting the aged gut microbiome to a more youthful state produces benefits to health.

As is now well known, the gut microbiome changes with age in ways that cause harm to long-term health. The reasons for this change are not fully understood, but the age-related decline of the immune system, responsible for gardening the gut microbiome, may be an important factor. Beneficial microbial populations, such as those that generate useful metabolites, decline in number. Harmful populations increase in number, provoking chronic inflammation. Numerous animal studies have demonstrated that fecal microbiota transplantation from young individual to old individuals can produce a lasting improvement in the state of the gut microbiome. That is accompanied by improved health and, in some studies, extension of life span.

Regular fecal microbiota transplantation to Senescence Accelerated Mouse-Prone 8 (SAMP8) mice delayed the aging of locomotor and exploration ability by rejuvenating the gut microbiota

Recent evidence points out the role of the gut microbiota in the aging process. However, the specific changes and relevant interventions remain unclear. In this study, Senescence Accelerated Mouse-Prone 8 (SAMP8) mice were divided into four groups; young-FMT-group transplanted fecal microbiota from young donors (2-3 months old) and old-FMT-group transplanted from old donors (10-11 months old); additionally, other two groups, either adult mice injected with saline solution or untreated mice, served as the saline and blank control groups, respectively. All mice were intervened from their 7-months-old until 13-months-old.

The open field test conducted at 9 and 11 months of age showed that the mice transplanted with gut microbiota from young donors had significantly better locomotor and exploration ability than those of transplanted with old-donors gut microbiota and those of saline control while was comparable with the blank control. 16S rRNA gene sequencing showed that the gut microbiome of recipient mice of young donors was altered at 11 months of age, whereas the alteration of the gut microbiome of old-donor recipient mice was at 9 months. For comparison, the recipient mice in the blank and saline control groups exhibited changes in the gut microbiome at 10 months of age.

The hallmark of aging-related gut microbiome change was an increase in the relative abundance of Akkermansia, which was significantly higher in the recipients transplanted with feces from older donors than younger donors at 9 months of age. This study shows that fecal microbiota transplantation from younger donors can delay aging-related declines in locomotor and exploration ability in mice by changing the gut microbiome.