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Probiotics protect against ALS in a worm model

Probiotics protect against ALS in a worm model

 


Scientists at CRCHUM have discovered that a bacterium called Lacticaseibacillus rhamnosus HA-114 prevents neurodegeneration. Nematode A worm used to study amyotrophic lateral sclerosis.

A probiotic bacterium called Lacticaseibacillus rhamnosus HA-114 prevents neurodegeneration. Nematode Worms, an animal model used to study amyotrophic lateral sclerosis (ALS).

that’s the discovery new research at the Canadian Center for Research CHUM (CRCHUM), led by a professor of neuroscience at the University of Montreal Alex Parker and published in magazines communication biology.

He and his team suggest that disruption of lipid metabolism contributes to this brain degeneration, suggesting that the neuroprotection provided by HA-114, a non-commercial probiotic, could be attributed to the same bacterial family tested. This indicates that it is unique compared to other strains of .

“We find that adding it to the diet in our animal model slows down the progression of motor neuron degeneration,” said Parker, the lead author of the study. “HA-114 is characterized by its fatty acid content.”

Motor neurons, which are nerve cells, give our bodies the freedom to move by sending signals to muscles to contract them.

Patients with ALS show a gradual deterioration of motor neurons. This causes them to lose muscle capacity and become completely paralyzed, with a life expectancy of only 3-5 years after diagnosis.

About 3,000 people in Canada have ALS.

“Recent studies have shown that disruption of the gut microbiota likely plays a role in the development and progression of many incurable neurodegenerative diseases, including ALS,” explained Parker. I’m here.

Identifying neuroprotective bacterial strains may be the basis for new therapies.

food problems

Central to this scientific project is the Audrey LavalThe study’s first author and postdoctoral fellow, he works hard to advance ALS research with a focus on motor neuron degeneration in the United States. Nematode worm.

These nematodes, which are only 1 mm long and share 60% of their genetic makeup with humans, were genetically engineered with ALS-associated genes for the purpose of CRCHUM studies.

To study the neuroprotective effects of probiotic-based dietary supplements on this animal model, Labarre tested a total of 13 different bacterial strains and 3 strain combinations.

HA-114 was by far the best. The action of probiotics has helped reduce movement disorders in models of ALS and Huntington’s disease, another neurodegenerative disease.

two genes at work

Relying on data from genetic studies, genomic profiling, behavioral analyses, and microscopic imaging, the scientific team identified two genes, acdh-1 and acs-20, that play critical roles in this neuroprotective mechanism.

They are, Martine Tetroa CRCHUM researcher, and Matthieu Ruiz, a researcher at the Montreal Heart Institute Research Center.

Both genes, present in equivalent forms in humans, are involved in lipid metabolism and beta-oxidation, the processes by which fatty acids are broken down into energy in mitochondria, the true cellular powerhouses.

“We believe that fatty acids supplied by HA-114 enter mitochondria via independent and unconventional pathways,” said Parker. In doing so, it restores the balance of the impaired energy metabolism in ALS, leading to a reduction in neurodegeneration. “

The research team is now conducting similar studies in mice, a more complex animal model than the C. elegans worm.

It will then be tested in clinical settings to see if HA-114 could be a complementary therapy to current ALS treatments. The advantage of probiotics is that unlike drugs, they have few side effects.

To this end, headquartered at CRCHUM, Director of the ALS Clinic Dr. Genevieve Matte will be implemented in 100 subjects from spring 2023.

reference: Fatty acids from Labarre A, Guitard E, Tossing G and other probiotics Lactica seibacillus rhamnosus HA-114 inhibits age-related neurodegeneration. symbiote2022;5(1):1-19. Doi: 10.1038/s42003-022-04295-8

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