Obesity has become a global epidemic and a public health crisis in the Western World, experiencing a threefold increase in prevalence since 1975. High-caloric diets and sedentary lifestyles have been identified as significant contributors to this widespread issue, although the role of genetic, social, and environmental factors in obesity’s pathogenesis remain incompletely understood. In recent years, much attention has been drawn to the contribution of the gut microbiota in the development of obesity. Indeed, research has shown that in contrast to their healthier counterparts the microbiomes of obese individuals are structurally and functionally distinct, strongly suggesting microbiome as a potential target for obesity therapeutics. In particular, pre and probiotics have emerged as effective and integrative means of modulating the microbiome, in order to reverse the microbial dysbiosis associated with an obese phenotype. The following review brings forth animal and human research supporting the myriad of mechanisms by which the microbiome affects obesity, as well as the strengths and limitations of probiotic or prebiotic supplementation for the prevention and treatment of obesity. Finally, we set forth a roadmap for the comprehensive development of functional food solutions in combatting obesity, to capitalize on the potential of pre/probiotic therapies in optimizing host health.

The Microbiome has generated significant attention for its impacts not only on gastrointestinal health, but also on signaling pathways of the enteric and central nervous system via the microbiome gut–brain axis. In light of this, microbiome modulation may be an effective therapeutic strategy for treating or mitigating many somatic and neural pathologies, including neurodegenerative disorders. Alzheimer’s disease (AD) is a chronic neurodegenerative disease that interferes with cerebral function by progressively impairing memory, thinking and learning through the continuous depletion of neurons. Although its etiopathogenesis remains uncertain, recent literature endorses the hypothesis that probiotic, prebiotic and synbiotic supplementation alters AD-like symptoms and improves many of its associated disease biomarkers. Alternatively, a dysfunctional microbiota impairs the gut epithelial barrier by inducing chronic gastric inflammation, culminating in neuroinflammation and accelerating AD progression. The findings in this review suggest that probiotics, prebiotics or synbiotics have potential as novel biological prophylactics in treatment of AD, due to their anti-inflammatory and antioxidant properties, their ability to improve cognition and metabolic activity, as well as their capacity of producing essential metabolites for gut and brain barrier permeability.