2. Academic Validation
  3. Fatty acids derived from the probiotic Lacticaseibacillus rhamnosus HA-114 suppress age-dependent neurodegeneration

Fatty acids derived from the probiotic Lacticaseibacillus rhamnosus HA-114 suppress age-dependent neurodegeneration

  • Commun Biol. 2022 Dec 7;5(1):1340. doi: 10.1038/s42003-022-04295-8.
Audrey Labarre 1 2,  Ericka Guitard 1 2,  Gilles Tossing 1 2,  Anik Forest 3,  Eric Bareke 2,  Marjorie Labrecque 2 4,  Martine Tétreault 1 2,  Matthieu Ruiz 3 5,  J Alex Parker 6 7
Affiliations

Affiliations

  • 1 Département de Neurosciences, Université de Montréal, Montréal, QC, Canada.
  • 2 Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montréal, QC, Canada.
  • 3 Centre de Recherche, Institut de Cardiologie de Montréal, Montréal, QC, Canada.
  • 4 Département de Biochimie, Université de Montréal, Montréal, QC, Canada.
  • 5 Département de Nutrition, Université de Montréal, Montréal, QC, Canada.
  • 6 Département de Neurosciences, Université de Montréal, Montréal, QC, Canada. ja.parker@umontreal.ca.
  • 7 Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montréal, QC, Canada. ja.parker@umontreal.ca.
PMID: 36477191 DOI: 10.1038/s42003-022-04295-8
Abstract

The human microbiota is believed to influence health. Microbiome dysbiosis may be linked to neurological conditions like Alzheimer's disease, amyotrophic lateral sclerosis, and Huntington's disease. We report the ability of a probiotic Bacterial strain in halting neurodegeneration phenotypes. We show that Lacticaseibacillus rhamnosus HA-114 is neuroprotective in C. elegans models of amyotrophic lateral sclerosis and Huntington's disease. Our results show that neuroprotection from L. rhamnosus HA-114 is unique from other L. rhamnosus strains and resides in its fatty acid content. Neuroprotection by L. rhamnosus HA-114 requires acdh-1/ACADSB, kat-1/ACAT1 and elo-6/ELOVL3/6, which are associated with fatty acid metabolism and mitochondrial β-oxidation. Our data suggest that disrupted lipid metabolism contributes to neurodegeneration and that dietary intervention with L. rhamnosus HA-114 restores lipid homeostasis and energy balance through mitochondrial β-oxidation. Our findings encourage the exploration of L. rhamnosus HA-114 derived interventions to modify the progression of neurodegenerative diseases.

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