Protective probiotic discovered for ALS

Protective probiotic discovered for ALS

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Summary: Lacticaseibacillus rhamnosus HA-114, a non-commercial probiotic reduces neurodegeneration and has neuroprotective effects in laboratory models of ALS.

source: University of Montreal

A probiotic bacterium called Lacticaseibacillus rhamnosus HA-114 prevents neurodegeneration in the worm C. elegans, an animal model used to study amyotrophic lateral sclerosis (ALS).

This is the finding of a new study at the Canadian Research Center CHUM (CRCHUM), led by University of Montreal neuroscience professor Alex Parker and published in the journal Biology of Communications.

He and his team hypothesize that disruption of lipid metabolism contributes to this cerebral degeneration and show that the neuroprotection provided by HA-114, a non-commercial probiotic, is unique compared to other strains of the same bacterial family tested.

“When we add it to the diet of our animal model, we notice that it suppresses the progression of motor neuron degeneration,” said Parker, the study’s lead author. “The specialty of HA-114 lies in its fatty acid content.”

By allowing signals to be transmitted to muscles so that they contract, motor neurons, which are nerve cells, allow us to move our bodies at will.

People with ALS see a gradual deterioration of their motor neurons. This causes them to lose their muscle power to the point of complete paralysis, with an average life expectancy of only 3 to 5 years after diagnosis.

Nearly 3,000 people in Canada have ALS.

“Recent research suggests that disruption of the gut microbiota is likely linked to the onset and progression of many incurable neurodegenerative diseases, including ALS,” Parker explained.

The identification of neuroprotective bacterial strains may form the basis for new therapies.

A matter of diet

At the center of this scientific project is Audrey Labar, the study’s first author, a postdoctoral fellow who has worked hard to advance ALS research by focusing on motor neuron degeneration in C. elegans worms.

Measuring just one millimeter in length and sharing 60% of their genetic makeup with humans, these nematodes were genetically modified with ALS-related genes for the purposes of the CRCHUM study.

To study the neuroprotective effects of a probiotic dietary supplement in this animal model, Labarre tested a total of 13 different bacterial strains and three combinations of strains.

The HA-114 stood out from the pack. The action of the probiotic helped reduce movement disorders in models of ALS and also Huntington’s disease, another neurodegenerative disease.

Two genes at play

Using data from genetic testing, genomic profiling, behavioral analysis, and microscopic imaging, the research team identified two genes, acdh-1 and acs-20, that play a key role in this neuroprotective mechanism.

Mechanism of neuroprotection of Lacticaseibacillus rhamnosus HA-114. ALS models have impaired carnitine shuttle, a mechanism for transporting long-chain fatty acids across the mitochondrial membrane for energy production by β-oxidation. Fatty acids supplied by probiotic bacteria are thought to enter mitochondria independently of the carnitine shuttle to participate in several rounds of β-oxidation, which helps stabilize energy metabolism, leading to reduced neurodegeneration and improved lipid homeostasis. Created with Credit: The researchers

They were able to carry out this meticulous work thanks to the collaboration with Martine Tétreault, a researcher at CRCHUM, and Matthieu Ruiz, a researcher at the Research Center of the Montreal Heart Institute.

Existing in equivalent forms in humans, both genes are involved in lipid metabolism and beta-oxidation, the process by which fatty acids are broken down for energy in mitochondria, the true cellular powerhouses.

“We believe that the fatty acids delivered by HA-114 enter the mitochondria through an independent, unconventional pathway,” Parker said. In this way, they restore the balance of disturbed energy metabolism in ALS and lead to a reduction of neurodegeneration.

The researcher’s team is now conducting similar studies in an animal model more complex than the C. elegans worm: the mouse.

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They will then confirm in a clinical setting whether HA-114 can be a therapeutic addition to current ALS treatments. The advantage is that probiotics, unlike drugs, cause few side effects, they say.

To this end, a Canada-wide clinical trial based at CRCHUM and led by ALS Clinic Director Dr. Geneviève Matte will be conducted with 100 subjects starting in spring 2023.

About this ALS research news

Author: Bruno Geoffroy
source: University of Montreal
Contact: Bruno Geoffroy – University of Montreal
Image: Image is credited to the researchers

Original Research: Free access.
Fatty acids derived from the probiotic Lacticaseibacillus rhamnosus HA-114 suppress age-related neurodegeneration” by Audrey Labar et al. Biology of Communications


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

The human microbiota is thought to influence health. Microbiome dysbiosis may be linked to neurological conditions such as Alzheimer’s disease, amyotrophic lateral sclerosis, and Huntington’s disease. We report the ability of a probiotic bacterial strain to arrest neurodegenerative 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 by L. rhamnosus HA-114 is unique from others L. rhamnosus strains and contained in the fatty acid content.

Neuroprotection from L. rhamnosus HA-114 requires acdh-1/ACADSB, cat-1/ACAT1 and elo-6/ELOVL3/6, which are related to fatty acid metabolism and mitochondrial β-oxidation. Our data show that impaired 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 study of L. rhamnosus HA-114-derived interventions to modify the progression of neurodegenerative diseases.

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