From Dysbiosis to Neurodegenerative Diseases through Different Communication Pathways: An Overview

Simple Summary For millennia, humankind has had a symbiotic relationship with different bacterial species, called the microbiota. Our microbiota can affect the homeostasis, the health status and the various functions of our body. In this paper, correlations between gut microbiota (GM) and several neurodegenerative processes will be analyzed. We focus our analysis on the possible alterations to the GM (dysbiosis) and their consequences on the human nervous system. Generally, there is an exchange of molecules between the bacterial and the nervous cell populations. An alteration of this communication can evolve into a range of pathological conditions. The present analysis covers the different altered molecular mechanisms and the pathological states observed in conjunction with them. The knowledge of these mechanisms could lead to the development of new therapeutic targets that could counteract neuroinflammation and neurodegeneration. The microbiome research field has rapidly evolved over the last few decades, becoming a major topic of scientific and public interest. The gut microbiota (GM) is the microbial population living in the gut. The GM has many functions, such as maintaining gut homeostasis and host health, providing defense against enteric pathogens, and involvement in immune system development. Several studies have shown that GM is implicated in dysbiosis and is presumed to contribute to neurodegeneration. This review focuses mainly on describing the connection between the intestinal microbiome alterations (dysbiosis) and the onset of neurodegenerative diseases to explore the mechanisms that link the GM to nervous system health, such as the gut-brain axis, as well as the mitochondrial, the adaptive humoral immunity, and the microvesicular pathways. The gut-brain communication depends on a continuous bidirectional flow of molecular signals exchanged through the neural and the systemic circulation. These pathways represent a possible new therapeutic target against neuroinflammation and neurodegeneration. Progress in this context is desperately needed, considering the severity of most neurodegenerative diseases and the current lack of effective treatments.