Gut microbiota dysbiosis motor deficits and neuroinflammation in a model of parkinson's disease

Gut microbiota dysbiosis motor deficits and neuroinflammation in a model of parkinson's disease

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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 Reprints 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 Download citation * Published: 16 December 2016 * Issue Date: 16 December 2016 * DOI: https://doi.org/10.1038/sj.bdj.2016.949 SHARE THIS ARTICLE Anyone you share the following link with will be able to read this content: Get shareable link Sorry, a shareable link is not currently available for this article. Copy to clipboard Provided by the Springer Nature SharedIt content-sharing initiative

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 Reprints 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 Download citation * Published: 16 December 2016 * Issue Date:


16 December 2016 * DOI: https://doi.org/10.1038/sj.bdj.2016.949 SHARE THIS ARTICLE Anyone you share the following link with will be able to read this content: Get shareable link Sorry, a


shareable link is not currently available for this article. Copy to clipboard Provided by the Springer Nature SharedIt content-sharing initiative