Preclinical and human studies have demonstrated the link between unbalanced gut microbiota and Alzheimer’s Disease (AD). However, there is still a lot of debate about how metabolic pathways are involved. Evidence indicates that neurodegenerative disorders are often associated with metabolic dysfunction, such as deregulation of lipid homeostasis, which may worsen neurological symptoms and contribute to AD progression. However, mechanistic insights into the link between abnormal lipid metabolism and beta-amyloid aggregation and clearance are unavailable.
Several studies describe the cholesterol-lowering effects of probiotics in both animals and humans. Bonfili and colleagues explored the effects of Slab51 on lipid metabolism in a mice model of the disease(1). Previous results from the team demonstrated that long-term supplementation with Slab51 in 3xTg-AD mice positively affected glucose metabolism, inflammatory and oxidative status and partially recovered the impaired neuronal proteolysis, finally improving cognitive abilities, with the consequent delay of AD progression (2-4).
This most recent work published in Clinical Nutrition investigated how microbiota modulation through probiotics can affect lipid composition in the same animal model. Results showed that Slab51 inhibited hepatic lipogenesis and cholesterol biosynthesis and qualitatively improved plasma lipid composition, consequently reducing total cholesterol/HDL-C and LDL-C/HDL-C ratios. The authors highlighted a plasmatic increase in arachidonic acid representing one key metabolite in the interactions among probiotic-induced lipid profile changes, insulin sensitivity, and inflammation.
This specific probiotic formulation also ameliorated the omega6/omega3 ratio, which results in unbalanced during inflammation-associated diseases, such as diabetes, obesity, mental disorders, cardiovascular and autoimmune diseases.