GRAU roberto Ricardo
Bacillus Subtilis Delays Neurodegeneration and Behavioral Impairment in the Alzheimer?s Disease Model Caenorhabditis Elegans
COGLIATI S.; CLEMENTI V.; FRANCISCO M; CIRA CRESPO; ARGAÑARAZ F.; GRAU R.
Journal of Alzheimer Disease
Año: 2020 vol. 73 p. 1035 - 1052
Multiple causes, apart from genetic inheritance, predispose to the production and aggregation of amyloid- (A)peptide and Alzheimer?s disease (AD) development in the older population. There is currently no therapy or medicine toprevent or delay AD progression. One novel strategy against AD might involve the use of psychobiotics, probiotic gut bacteriawith specific mental health benefits. Here, we report the neuronal and behavioral protective effects of the probiotic bacteriumBacillus subtilis in a Caenorhabditis elegans AD model. Aging and neuronal deterioration constitute important risk factorsfor AD development, and we showed that B. subtilis significantly delayed both detrimental processes in the wild-type C.elegans strain N2 compared with N2 worms colonized by the non-probiotic Escherichia coli OP50 strain. Importantly, B.subtilis alleviated the AD-related paralysis phenotype of the transgenic C. elegans strains CL2120 and GMC101 that express,in body wall muscle cells, the toxic peptides A3-42 and A1-42, respectively. B. subtilis-colonized CL2355 worms wereprotected from the behavioral deficits (e.g., poor chemotactic response and decreased body bends) produced by pan-neuronalA1-42 expression. Notably, B. subtilis restored the lifespan level of C. elegans strains that express A to values similar tothe life expectancy of the wild-type strain N2 fed on E. coli OP50 cells. The B. subtilis proficiencies in quorum-sensingpeptide (i.e., the Competence Sporulation Factor, CSF) synthesis and gut-associated biofilm formation (related to the antiagingeffect of the probiotic) play a crucial role in the anti-AD effects of B. subtilis. These novel results are discussedin the context of how B. subtilis might exert its beneficial effects from the gut to the brain of people with or at risk ofdeveloping AD.