A selection of abstracts of clinically relevant papers from other journals. The abstracts on this page have been chosen and edited by John R. Radford.
Abstract
'Signals from gut microbes are required for the neuroinflammatory responses...in Parkinson's disease.'
Main
Sampson TR, Debelius JW et al. Cell 2016; 167: 1469–1480
A recent article (Br Dent J 2016; 221: 657–666) focused on dysbiosis; this is when the 'normal microbiome population structure is disturbed, often through external burdens such as disease states or medications'. Dysbiosis in the oral cavity could be fundamental in the aetiology of both dental caries and periodontal diseases. This paper published in Cell comprises a succinct graphical Abstract and Highlights, an overview of the elegant experiments that explore Braak's hypothesis and details of the methods used in these experiments. As background, it is hypothesised that Parkinson's disease is because of dysbiosis in the gut; 'Braak's hypothesis posits that aberrant aSyn (alpha-synuclein) accumulation initiates in the gut and propagates via nerve to the brain in a prion-like fashion'. One of the experiments published in Cell describes germ-free mice that had been genetically modified to overproduce alpha-synuclein maintain motor skills, but similar mice with a gut microbiome showed brain damage. In another experiment, mice developed enhanced motor dysfunction when samples of gut bacteria from humans with Parkinson's disease were transplanted into germ-free mice that overexpressed alpha-synuclein, but other mice who were inoculated with gut bacteria from humans without Parkinson's disease did not develop disease.
Rights and permissions
About this article
Cite this article
Gut microbiota dysbiosis motor deficits and neuroinflammation in a model of Parkinson's Disease. Br Dent J 221, 772 (2016). https://doi.org/10.1038/sj.bdj.2016.949
Published:
Issue Date:
DOI: https://doi.org/10.1038/sj.bdj.2016.949