Abstract
Canine cognitive dysfunction (CCD) is the dog version of human Alzheimer's disease (AD), and it has strikingly similar pathological features to those of this neurodegenerative disorder. The gastrointestinal system is in constant communication with the brain via several conduits collectively termed the gut-brain axis. The microbial population of the gut, referred to as the microbiota, has a profound effect on the interactions that occur along this communication route. Recent evidence suggests that dysbiosis, an abnormal gastrointestinal microbial population, is linked to cognitive impairment in rodent AD models and human AD. There is also evidence from rodent AD models that correcting dysbiosis by transferring fecal material from healthy donors to the gastrointestinal tracts of cognitively impaired recipients [fecal microbiome transplantation (FMT)] reverses AD-associated brain pathology and improves cognitive function. Although limited, some clinical reports have described the improvement of cognitive function with FMT in human AD. The goals of this review article are to provide an overview of the mechanisms involved in dysbiosis- associated cognitive decline and the role of FMT in therapy for such decline. The potential role of FMT in CCD is also discussed.