Gastrointestinal (GI) bacteria, fungi, viruses, and parasites are referred to as the ‘microbiota’ or ‘microbiome.’ Fungi or the mycobiome, alongside the bacteriome, play key roles in establishing the synergism of the gut and, therefore, cannot be ignored. The Nobel laureate Elie Metchnikoff postulated that the good bacteria of the gut, referred to as probiotics, benefit the host in myriad ways. However, it is pertinent to note that the coexistence of probiotics with fungal members is essential in maintaining the conducive probiotic-induced benefits. This is the basis of fecal transplantation, which involves the administration of the microbiome from healthy subjects to diseased individuals. Our previous findings suggest a synergistic association between the bacteriome and mycobiome, the dynamics of which depend on numerous factors such as antibiotic usage, stress, infection, and other metabolic and environmental factors. We compared mycobiome with changing bacteriome pre- and post-antibiotics and pre- and post-fecal microbiome transplant (FMT). Our findings have also revealed a possible role of amylin (a peptide hormone associated with type 2 diabetes) in association with amyloid plaques. In this study, we propose aims to address this area with emphasis on how some of the above factors induce changes in microbiome profile and how that impacts the brain in Alzheimer’s disease (AD) using mouse models that were not used in our earlier studies. In this study, we will continue working on our previous aims and investigating the possible role of amylin in the gut-brain axis that has opened new doors to a novel synergistic mechanism involving amyloid beta and amylin in the brain. Findings also raise an exciting possibility that these two antimicrobial peptides (amylin’s antimicrobial role is ready for publication) may be functioning in concert with each other as the brain’s innate defense. We will use novel AD mouse models to investigate the emergence of specific fungal genera and species in relation to bacteria that emerge post-antibiotic treatment and how this change might be linked to amylin in mitigating or accelerating CNS insult. Findings are likely to provide a better understanding of designing novel strategies for the early treatment of AD.
