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Scientists discover bacteria behind neuro-degenersative diseases

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Scientists discover bacteria behind neuro-degenersative diseases

Alzheimer’s, dementia, Parkinson’s and motor neurone disease stem from changes to a healthy gut microbiome, according to University of Florida researchers and the Short-chain Fatty Acid (SFA) butyrate seems able to correct this.

According to Assistant Professor Dr. Daniel Czyz, the researchers found bacteria strains that caused the diseases, and others that could correct.

Using worms (C elegans) they showed that certain enteric bacterial pathogens disrupted the formation of certain proteins in the gut and instead caused the build-up of toxic proteins in their bodies and these proteins aggregated, while other bacteria that made butyrate could return normal protein synthesis to the gut. 

Butyrate has previously been shown to have an impact on neurodegenerative diseases but no one knew exactly why. 

Also, previous studies have shown that protein structures built up in the gut of Alzheimer’s patients prompting immune attack on these structures. The problem is that these structures strongly resemble amyloid plaque structures in the brain and so these are simultaneously attacked by the same immune system activity. Butyrate-producing bacteria seem capable of preventing this. 

Butyrate, along with propionate and acetate are Short-chain Fatty Acids (SFAs) increasingly understood to be produced by ‘super gut bacteria’ since these SFAs perform so many critical functions in the body, from blocking cholesterol formation to killing cancer cells.

Go to: Increasing evidence of Gut bacterial involvement in Parkinson’s Disease

Go to: Gut bacteria play key role in Alzheimer’s and dementia

Go to: Butyrate significantly improves your health

Reference

  1. Walker AC, Bhargava R, Vaziriyan-Sani AS, Pourciau C, Donahue ET, Dove AS, et al. (2021) Colonization of the Caenorhabditis elegans gut with human enteric bacterial pathogens leads to proteostasis disruption that is rescued by butyrate. PLoS Pathog 17(5): e1009510. doi:10.1371/journal.ppat.1009510