Unique probiotic may prevent neurodegeneration and restore lipid balance in amyotrophic lateral sclerosis

By restoring lipid homeostasis and energy balance through mitochondrial-oxidation, dietary supplementation of unique probiotic containing L. rhamnosus HA-114 prevents neurodegeneration and disturbed lipid metabolism in amyotrophic lateral sclerosis.

The study has been published in Communications Biology.

It is thought that the human microbiome affects health. Neurological disorders including Alzheimer's disease, amyotrophic lateral sclerosis, and Huntington's disease may be associated with microbiome dysbiosis. In this work, Audrey Labarre and colleagues describe how a probiotic bacterial strain can stop the hallmarks of neurodegeneration. Additionally demonstrated to be neuroprotective in C. elegans models of Huntington's disease and amyotrophic lateral sclerosis is lacticaseibacillus rhamnosus HA-114.

The bacterium Lacticaseibacillus rhamnosus HA-114 is present in the probiotic. 13 distinct bacterial strains and three strain combinations were examined by the researchers. HA-114 stood out among the other models. Animal models for amyotrophic lateral sclerosis (ALS) or Huntington's illness experienced less motor abnormalities according to the probiotic's effect. The group discovered two genes involved in mitochondrial -oxidation and fatty acid metabolism that looked to be crucial in this neuroprotective process.

Further findings demonstrate that L. rhamnosus HA-114's neuroprotection is distinct from that of other L. rhamnosus strains and is due to the presence of fatty acids in the organism. The fatty acid metabolism and mitochondrial -oxidation-related genes acdh-1/ACADSB, kat-1/ACAT1, and elo-6/ELOVL3/6 are necessary for L. rhamnosus HA-114 to protect neurons.

In conclusion, according to research, fatty acids delivered by HA-114 enter the mitochondria by a distinct, unusual mechanism. Thus, they reduce neurodegeneration and restore equilibrium to the ALS-related altered energy metabolism. The results may motivate the investigation of interventions generated from L. rhamnosus HA-114 to slow the course of neurodegenerative illnesses and serve as a therapeutic supplement to existing ALS therapies. In a clinical trial involving 100 participants that will start in the spring of 2023, the research team intends to examine the therapy.

Reference:

Labarre, A., Guitard, E., Tossing, G., Forest, A., Bareke, E., Labrecque, M., Tétreault, M., Ruiz, M., & Alex Parker, J. (2022). Fatty acids derived from the probiotic Lacticaseibacillus rhamnosus HA-114 suppress age-dependent neurodegeneration. In Communications Biology (Vol. 5, Issue 1). Springer Science and Business Media LLC. https://doi.org/10.1038/s42003-022-04295-8