A good deal of research of late has focused on the role of the gut microbiome in aging. One portion of this part of the field covers the interactions between the gut microbiome and the brain. For example, butyrate is a metabolite generated by the gut microbiome, in declining amounts with age as the balance of microbial populations shifts. Butyrate upregulates BDNF, which in turn upregulates neurogenesis in the brain, the production of new neurons. The consensus on neurogenesis is that more of it is a good thing, and many research programs are working towards safe ways to achieve this goal.
One of the more notable age-related changes in the gut microbiome is the growth of inflammatory populations, those that provoke the immune system and cause a meaningful fraction of the chronic inflammation that is characteristic of older individuals. This inflammation contributes to the onset and progression of all of the common age-related conditions. Since the immune system is responsible for gardening the microbiome and removing these inflammatory microbes, this is a bidrectional relationship. More inflammatory microbes degrade the effectiveness of the immune system, but the dysfunctions of immune aging allow these harmful populations to run amok.
What can be done about this? In animal studies, fecal microbiota transplantation from young individuals to old individuals has been shown to reset the gut microbiome, improve health, and extend life. There are other strategies with varying degrees of evidence to support their efficacy, but this one seems the most practical, given that fecal microbiota transplantation is already used in medical practice, and thus it would be a comparatively small step to adapt it to this new use case.
It has been noticed in recent years that the unfavorable effects of the gut microbiota could exhaust host vigor and life, yet knowledge and theory are just beginning to be established. Increasing documentation suggests that the microbiota-gut-brain axis not only impacts brain cognition and psychiatric symptoms but also precipitates neurodegenerative diseases, such as Alzheimer's disease (AD).
How the blood-brain barrier (BBB), a machinery protecting the central nervous system (CNS) from the systemic circulation, allows the risky factors derived from the gut to be translocated into the brain seems paradoxical. For the unique anatomical, histological, and immunological properties underpinning its permeable dynamics, the BBB has been regarded as a biomarker associated with neural pathogenesis. The BBB permeability of mice and rats caused by GM dysbiosis raises the question of how the GM and its metabolites change BBB permeability and causes neuroinflammation and neurodegeneration (NF&ND) and brain aging, a pivotal multidisciplinary field tightly associated with immune and chronic systemic inflammation.
Gut microbiota-induced systemic chronic inflammation mainly refers to excessive gut inflammation caused by gut mucosal immunity dysregulation, which is often influenced by dietary components and age, is produced at the interface of the intestinal barrier (IB) or exacerbated after IB disruption, initiates various common chronic diseases along its dispersal routes, and eventually impairs BBB integrity to cause NF&ND and brain aging.