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Grompone, G., Martorell, P., Llopis, S., González, N., Genovés, S., Mulet, A.P., Fernández-Calero, T., Tiscornia, I., Bollati-Fogolín, M., Chambaud, I., Foligné, B., Montserrat, A. and Ramón, D. (2012) Anti-Inflammatory Lactobacillus rhamnosus CNCM I-3690 Strain Protects against Oxidative Stress and Increases Lifespan in Caenorhabditis elegans. PLoS ONE, 12, e52493.
http://dx.doi.org/10.1371/journal.pone.0052493

has been cited by the following article:

• TITLE: Dual PINK Mutant and Aβ42-Dependent Lifespan Shorten and Flight Impairment in Transgenic Drosophila Partially Alleviates by a Lactococcus lactis Supplemented Diet

  AUTHORS: Dong Gyun Ko, Young Bum Eun, Jong Uk Na, Sang-Tae Kim

  KEYWORDS: Drosophila melanogaster, Lactococcus lactis, PINK1, Lifespan, Ommatidia, Aβ42

  JOURNAL NAME: Journal of Behavioral and Brain Science, Vol.5 No.7, July 10, 2015

  ABSTRACT: Oxidative stress has been strongly related with Parkinson disease (PD) and Alzheimer disease pathogenesis. We determined the effects of Lactococcus lactis (LAL) supplementation on the generated loss-of-function mutants of PINK1 B9, an AR-JP-linked gene and Aβ42 induced phenotypes in a Drosophila melanogaster model of PD/AD. Enhanced mutant PINK1 B9 and Aβ42 expression in D. melanogaster dopaminergic (DA) neurons can curtail lifespan, flight muscle accompanied by locomotive defects and we have observed longevity methods to assay the effects of LAL on D. melanogaster survival. Furthermore, flies expressing mutant PINK1 B9 and Aβ42 in their brain fed LAL had up to the two weeks, or 25%, greater median lifespan than those fed a standard sucrose diet. In addition, LAL improved mutant PINK1 B9 and Aβ42-induced flight impairments in the Drosophila wing. Our microscopy analyses revealed that individuals fed LAL had improved atypical ommatidia as well as an increased thirteen percentage of flight ability than those fed a control diet. We propose that LAL, rich in naturally occurring probiotics and antioxidants, promotes the survival of neurons in brain and wing muscle tissues with increased levels of mutant PINK1 B9 and Aβ42 via a protective cell survival mechanism.