Gut microbiota are related to Parkinson's disease and clinical phenotype
In the course of Parkinson's disease (PD), the enteric nervous system (ENS) and parasympathetic nerves are amongst the structures earliest and most frequently affected by alpha‐synuclein pathology. Accordingly, gastrointestinal dysfunction, in particular constipation, is an important non‐motor...
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| Vydáno v: | Movement disorders Ročník 30; číslo 3; s. 350 - 358 |
|---|---|
| Hlavní autoři: | , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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United States
Blackwell Publishing Ltd
01.03.2015
Wiley Subscription Services, Inc |
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| ISSN: | 0885-3185, 1531-8257, 1531-8257 |
| On-line přístup: | Získat plný text |
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| Abstract | In the course of Parkinson's disease (PD), the enteric nervous system (ENS) and parasympathetic nerves are amongst the structures earliest and most frequently affected by alpha‐synuclein pathology. Accordingly, gastrointestinal dysfunction, in particular constipation, is an important non‐motor symptom in PD and often precedes the onset of motor symptoms by years. Recent research has shown that intestinal microbiota interact with the autonomic and central nervous system via diverse pathways including the ENS and vagal nerve. The gut microbiome in PD has not been previously investigated. We compared the fecal microbiomes of 72 PD patients and 72 control subjects by pyrosequencing the V1–V3 regions of the bacterial 16S ribosomal RNA gene. Associations between clinical parameters and microbiota were analyzed using generalized linear models, taking into account potential confounders. On average, the abundance of Prevotellaceae in feces of PD patients was reduced by 77.6% as compared with controls. Relative abundance of Prevotellaceae of 6.5% or less had 86.1% sensitivity and 38.9% specificity for PD. A logistic regression classifier based on the abundance of four bacterial families and the severity of constipation identified PD patients with 66.7% sensitivity and 90.3% specificity. The relative abundance of Enterobacteriaceae was positively associated with the severity of postural instability and gait difficulty. These findings suggest that the intestinal microbiome is altered in PD and is related to motor phenotype. Further studies are warranted to elucidate the temporal and causal relationships between gut microbiota and PD and the suitability of the microbiome as a biomarker. © 2014 International Parkinson and Movement Disorder Society |
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| AbstractList | In the course of Parkinson's disease (PD), the enteric nervous system (ENS) and parasympathetic nerves are amongst the structures earliest and most frequently affected by alpha-synuclein pathology. Accordingly, gastrointestinal dysfunction, in particular constipation, is an important non-motor symptom in PD and often precedes the onset of motor symptoms by years. Recent research has shown that intestinal microbiota interact with the autonomic and central nervous system via diverse pathways including the ENS and vagal nerve. The gut microbiome in PD has not been previously investigated. We compared the fecal microbiomes of 72 PD patients and 72 control subjects by pyrosequencing the V1-V3 regions of the bacterial 16S ribosomal RNA gene. Associations between clinical parameters and microbiota were analyzed using generalized linear models, taking into account potential confounders. On average, the abundance of Prevotellaceae in feces of PD patients was reduced by 77.6% as compared with controls. Relative abundance of Prevotellaceae of 6.5% or less had 86.1% sensitivity and 38.9% specificity for PD. A logistic regression classifier based on the abundance of four bacterial families and the severity of constipation identified PD patients with 66.7% sensitivity and 90.3% specificity. The relative abundance of Enterobacteriaceae was positively associated with the severity of postural instability and gait difficulty. These findings suggest that the intestinal microbiome is altered in PD and is related to motor phenotype. Further studies are warranted to elucidate the temporal and causal relationships between gut microbiota and PD and the suitability of the microbiome as a biomarker. copyright 2014 International Parkinson and Movement Disorder Society In the course of Parkinson's disease (PD), the enteric nervous system (ENS) and parasympathetic nerves are amongst the structures earliest and most frequently affected by alpha-synuclein pathology. Accordingly, gastrointestinal dysfunction, in particular constipation, is an important non-motor symptom in PD and often precedes the onset of motor symptoms by years. Recent research has shown that intestinal microbiota interact with the autonomic and central nervous system via diverse pathways including the ENS and vagal nerve. The gut microbiome in PD has not been previously investigated. We compared the fecal microbiomes of 72 PD patients and 72 control subjects by pyrosequencing the V1-V3 regions of the bacterial 16S ribosomal RNA gene. Associations between clinical parameters and microbiota were analyzed using generalized linear models, taking into account potential confounders. On average, the abundance of Prevotellaceae in feces of PD patients was reduced by 77.6% as compared with controls. Relative abundance of Prevotellaceae of 6.5% or less had 86.1% sensitivity and 38.9% specificity for PD. A logistic regression classifier based on the abundance of four bacterial families and the severity of constipation identified PD patients with 66.7% sensitivity and 90.3% specificity. The relative abundance of Enterobacteriaceae was positively associated with the severity of postural instability and gait difficulty. These findings suggest that the intestinal microbiome is altered in PD and is related to motor phenotype. Further studies are warranted to elucidate the temporal and causal relationships between gut microbiota and PD and the suitability of the microbiome as a biomarker. In the course of Parkinson's disease (PD), the enteric nervous system (ENS) and parasympathetic nerves are amongst the structures earliest and most frequently affected by alpha-synuclein pathology. Accordingly, gastrointestinal dysfunction, in particular constipation, is an important non-motor symptom in PD and often precedes the onset of motor symptoms by years. Recent research has shown that intestinal microbiota interact with the autonomic and central nervous system via diverse pathways including the ENS and vagal nerve. The gut microbiome in PD has not been previously investigated. We compared the fecal microbiomes of 72 PD patients and 72 control subjects by pyrosequencing the V1-V3 regions of the bacterial 16S ribosomal RNA gene. Associations between clinical parameters and microbiota were analyzed using generalized linear models, taking into account potential confounders. On average, the abundance of Prevotellaceae in feces of PD patients was reduced by 77.6% as compared with controls. Relative abundance of Prevotellaceae of 6.5% or less had 86.1% sensitivity and 38.9% specificity for PD. A logistic regression classifier based on the abundance of four bacterial families and the severity of constipation identified PD patients with 66.7% sensitivity and 90.3% specificity. The relative abundance of Enterobacteriaceae was positively associated with the severity of postural instability and gait difficulty. These findings suggest that the intestinal microbiome is altered in PD and is related to motor phenotype. Further studies are warranted to elucidate the temporal and causal relationships between gut microbiota and PD and the suitability of the microbiome as a biomarker. © 2014 International Parkinson and Movement Disorder Society In the course of Parkinson's disease (PD), the enteric nervous system (ENS) and parasympathetic nerves are amongst the structures earliest and most frequently affected by alpha-synuclein pathology. Accordingly, gastrointestinal dysfunction, in particular constipation, is an important non-motor symptom in PD and often precedes the onset of motor symptoms by years. Recent research has shown that intestinal microbiota interact with the autonomic and central nervous system via diverse pathways including the ENS and vagal nerve. The gut microbiome in PD has not been previously investigated. We compared the fecal microbiomes of 72 PD patients and 72 control subjects by pyrosequencing the V1-V3 regions of the bacterial 16S ribosomal RNA gene. Associations between clinical parameters and microbiota were analyzed using generalized linear models, taking into account potential confounders. On average, the abundance of Prevotellaceae in feces of PD patients was reduced by 77.6% as compared with controls. Relative abundance of Prevotellaceae of 6.5% or less had 86.1% sensitivity and 38.9% specificity for PD. A logistic regression classifier based on the abundance of four bacterial families and the severity of constipation identified PD patients with 66.7% sensitivity and 90.3% specificity. The relative abundance of Enterobacteriaceae was positively associated with the severity of postural instability and gait difficulty. These findings suggest that the intestinal microbiome is altered in PD and is related to motor phenotype. Further studies are warranted to elucidate the temporal and causal relationships between gut microbiota and PD and the suitability of the microbiome as a biomarker.In the course of Parkinson's disease (PD), the enteric nervous system (ENS) and parasympathetic nerves are amongst the structures earliest and most frequently affected by alpha-synuclein pathology. Accordingly, gastrointestinal dysfunction, in particular constipation, is an important non-motor symptom in PD and often precedes the onset of motor symptoms by years. Recent research has shown that intestinal microbiota interact with the autonomic and central nervous system via diverse pathways including the ENS and vagal nerve. The gut microbiome in PD has not been previously investigated. We compared the fecal microbiomes of 72 PD patients and 72 control subjects by pyrosequencing the V1-V3 regions of the bacterial 16S ribosomal RNA gene. Associations between clinical parameters and microbiota were analyzed using generalized linear models, taking into account potential confounders. On average, the abundance of Prevotellaceae in feces of PD patients was reduced by 77.6% as compared with controls. Relative abundance of Prevotellaceae of 6.5% or less had 86.1% sensitivity and 38.9% specificity for PD. A logistic regression classifier based on the abundance of four bacterial families and the severity of constipation identified PD patients with 66.7% sensitivity and 90.3% specificity. The relative abundance of Enterobacteriaceae was positively associated with the severity of postural instability and gait difficulty. These findings suggest that the intestinal microbiome is altered in PD and is related to motor phenotype. Further studies are warranted to elucidate the temporal and causal relationships between gut microbiota and PD and the suitability of the microbiome as a biomarker. |
| Author | Murros, Kari Eerola-Rautio, Johanna Kinnunen, Esko Scheperjans, Filip Koskinen, Kaisa Auvinen, Petri Paulin, Lars Haapaniemi, Elena Kaakkola, Seppo Aho, Velma Pereira, Pedro A. B. Pekkonen, Eero Pohja, Marjatta |
| Author_xml | – sequence: 1 givenname: Filip surname: Scheperjans fullname: Scheperjans, Filip email: filip.scheperjans@hus.fi organization: Department of Neurology, Helsinki University Central Hospital, and Department of Neurological Sciences, University of Helsinki, Helsinki, Finland – sequence: 2 givenname: Velma surname: Aho fullname: Aho, Velma organization: Institute of Biotechnology, DNA Sequencing and Genomics Laboratory, University of Helsinki, Helsinki, Finland – sequence: 3 givenname: Pedro A. B. surname: Pereira fullname: Pereira, Pedro A. B. organization: Institute of Biotechnology, DNA Sequencing and Genomics Laboratory, University of Helsinki, Helsinki, Finland – sequence: 4 givenname: Kaisa surname: Koskinen fullname: Koskinen, Kaisa organization: Institute of Biotechnology, DNA Sequencing and Genomics Laboratory, University of Helsinki, Helsinki, Finland – sequence: 5 givenname: Lars surname: Paulin fullname: Paulin, Lars organization: Institute of Biotechnology, DNA Sequencing and Genomics Laboratory, University of Helsinki, Helsinki, Finland – sequence: 6 givenname: Eero surname: Pekkonen fullname: Pekkonen, Eero organization: Department of Neurology, Helsinki University Central Hospital, and Department of Neurological Sciences, University of Helsinki, Helsinki, Finland – sequence: 7 givenname: Elena surname: Haapaniemi fullname: Haapaniemi, Elena organization: Department of Neurology, Helsinki University Central Hospital, and Department of Neurological Sciences, University of Helsinki, Helsinki, Finland – sequence: 8 givenname: Seppo surname: Kaakkola fullname: Kaakkola, Seppo organization: Department of Neurology, Helsinki University Central Hospital, and Department of Neurological Sciences, University of Helsinki, Helsinki, Finland – sequence: 9 givenname: Johanna surname: Eerola-Rautio fullname: Eerola-Rautio, Johanna organization: Department of Neurology, Helsinki University Central Hospital, and Department of Neurological Sciences, University of Helsinki, Helsinki, Finland – sequence: 10 givenname: Marjatta surname: Pohja fullname: Pohja, Marjatta organization: Department of Neurology, Helsinki University Central Hospital, and Department of Neurological Sciences, University of Helsinki, Helsinki, Finland – sequence: 11 givenname: Esko surname: Kinnunen fullname: Kinnunen, Esko organization: Department of Neurology, Hyvinkää Hospital, Hyvinkää, Finland – sequence: 12 givenname: Kari surname: Murros fullname: Murros, Kari organization: Department of Neurology, Helsinki University Central Hospital, and Department of Neurological Sciences, University of Helsinki, Helsinki, Finland – sequence: 13 givenname: Petri surname: Auvinen fullname: Auvinen, Petri organization: Institute of Biotechnology, DNA Sequencing and Genomics Laboratory, University of Helsinki, Helsinki, Finland |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25476529$$D View this record in MEDLINE/PubMed |
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Protein intake in parkinsonian patients using the EPIC food frequency question 2011; 479 2013; 29 1990; 53 1996; 39 2013; 28 2012; 486 2013; 2 2006; 32 2010; 464 2013; 20 2006; 130 2013; 125 2013; 70 1982; 143 2012; 19 2008; 105 2012; 16 2011; 17 2012; 13 2013; 8 2013; 5 2011; 473 2013; 19 2012; 72 1990; 40 2012; 70 2009; 13 2014; 5 2013; 16 2013; 11 1997; 10 2013; 98 2000; 59 2006; 21 2000; 57 2013; 50 2011; 68 2012; 27 2011; 26 2012; 336 2007; 22 2010; 5 2009; 15 2014; 11 2012; 62 2011; 258 2009; 25 2011; 334 2009; 24 2013; 109 2011 2013; 84 2013; 304 2014; 49 2008; 15 2013; 144 2006; 396 2008; 13 2013; 341 2011; 6 2014; 83 2009; 73 2011; 108 2012; 233 2014; 505 2009; 75 2004; 19 2003; 24 2009; 5 2014 2013 2009; 4 2011; 141 2003; 60 2012; 46 2012; 9 e_1_2_9_75_1 e_1_2_9_31_1 e_1_2_9_52_1 e_1_2_9_50_1 e_1_2_9_73_1 e_1_2_9_79_1 e_1_2_9_35_1 e_1_2_9_56_1 e_1_2_9_77_1 e_1_2_9_12_1 e_1_2_9_33_1 e_1_2_9_54_1 e_1_2_9_71_1 e_1_2_9_14_1 e_1_2_9_39_1 e_1_2_9_16_1 e_1_2_9_37_1 e_1_2_9_58_1 e_1_2_9_18_1 e_1_2_9_41_1 e_1_2_9_64_1 e_1_2_9_87_1 e_1_2_9_20_1 e_1_2_9_62_1 e_1_2_9_22_1 e_1_2_9_45_1 e_1_2_9_68_1 e_1_2_9_83_1 e_1_2_9_24_1 e_1_2_9_43_1 e_1_2_9_66_1 e_1_2_9_85_1 e_1_2_9_8_1 e_1_2_9_6_1 e_1_2_9_81_1 e_1_2_9_4_1 e_1_2_9_60_1 e_1_2_9_2_1 e_1_2_9_26_1 e_1_2_9_49_1 e_1_2_9_28_1 e_1_2_9_47_1 e_1_2_9_30_1 e_1_2_9_53_1 e_1_2_9_74_1 e_1_2_9_51_1 e_1_2_9_72_1 e_1_2_9_11_1 e_1_2_9_34_1 e_1_2_9_57_1 e_1_2_9_78_1 e_1_2_9_13_1 e_1_2_9_32_1 e_1_2_9_55_1 e_1_2_9_76_1 e_1_2_9_70_1 Korczyn AD (e_1_2_9_10_1) 1990; 53 e_1_2_9_15_1 e_1_2_9_38_1 e_1_2_9_17_1 e_1_2_9_36_1 e_1_2_9_59_1 e_1_2_9_19_1 e_1_2_9_42_1 e_1_2_9_63_1 e_1_2_9_88_1 e_1_2_9_40_1 e_1_2_9_61_1 e_1_2_9_21_1 e_1_2_9_46_1 e_1_2_9_67_1 e_1_2_9_84_1 e_1_2_9_23_1 e_1_2_9_44_1 e_1_2_9_65_1 e_1_2_9_86_1 e_1_2_9_7_1 e_1_2_9_80_1 e_1_2_9_5_1 e_1_2_9_82_1 e_1_2_9_3_1 e_1_2_9_9_1 e_1_2_9_25_1 e_1_2_9_27_1 e_1_2_9_48_1 e_1_2_9_69_1 e_1_2_9_29_1 25970839 - Mov Disord. 2015 Jul;30(8):1151 25545262 - Mov Disord. 2015 Mar;30(3):296-8 25534915 - Nat Rev Neurol. 2015 Feb;11(2):66 26095591 - Mov Disord. 2015 Jul;30(8):1151-3 |
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| Title | Gut microbiota are related to Parkinson's disease and clinical phenotype |
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