Diet, Gut Microbiome, and Cognitive Decline

Abstract

Purpose of review: An epidemic of age-associated cognitive decline, most commonly ascribed to neurodegenerative conditions such as Alzheimer's and Parkinson's disease, is causing healthcare costs to soar and devastating caregivers. An estimated 6.5 million Americans are living today with Alzheimer's disease, with 13.8 million cases projected by mid-century. Although genetic mutations are known to cause neurodegeneration, autosomal dominant disease is very rare and most sporadic cases can be attributed, at least in part, to modifiable risk factors.

Recent findings: Diet is a potential modifiable risk factor in cognitive decline. Food communicates with the brain through a complex signaling web involving multiple cells, mediators and receptors. Gut-brain communication is modulated by microorganisms including bacteria, archaea, viruses, and unicellular eukaryotes, which together constitute the microbiota. Microbes not only play major roles in the digestion and fermentation of the food, providing nutrients and bioactive metabolites, but also reflect the type and amount of food consumed and food-borne toxic exposures. Food components modify the diversity and abundance of the microbial populations, maintain the integrity of the gut barrier, and regulate the passage of microbes and their metabolites into the blood stream where they modulate the immune system and communicate with body systems including the brain. This paper will focus on selected mechanisms through which interactions between diet and the gut microbiota can modify brain integrity and cognitive function with emphasis on the pathogenesis of the most common dementia, Alzheimer's disease.

Keywords: Alzheimer’s disease; Amyloid; Copper; Dysbiosis; Flavonoids; Folate; Fructose; Gut microbiome; Gut-brain-axis signaling; Homocysteine; Hormesis; Hydrogen sulfide donors; Ketones; NAD; Polyphenols; Transsulfuration pathway; Vitamin B12; Vitamin B6.