Emerging evidences suggest that gut microbiota dysbiosis plays a role in Parkinson's disease (PD). However, the alterations in fecal microbiome in Chinese PD patients remains unknown. This case-control study was conducted to explore fecal microbiota compositions in Chinese PD patients. Microbiota communities in the feces of 45 patients and their healthy spouses were investigated using high-throughput Illumina Miseq sequencing targeting the V3-V4 region of 16S ribosomal RNA (rRNA) gene. The relationships between fecal microbiota and PD clinical characteristics were analyzed. The structure and richness of the fecal microbiota differed between PD patients and healthy controls. Genera Clostridium IV, Aquabacterium, Holdemania, Sphingomonas, Clostridium XVIII, Butyricicoccus and Anaerotruncus were enriched in the feces of PD patients after adjusting for age, gender, body mass index (BMI), and constipation. Furthermore, genera Escherichia/Shigella were negatively associated with disease duration. Genera Dorea and Phascolarctobacterium were negatively associated with levodopa equivalent doses (LED). Among the non-motor symptoms (NMSs), genera Butyricicoccus and Clostridium XlVb were associated with cognitive impairment. Overall, we confirmed that gut microbiota dysbiosis occurs in Chinese patients with PD. A well-controlled population involved was beneficial for the identification of microbiota associated with diseases. Additionally, the fecal microbiota was closely related to PD clinical characteristics. Elucidating these differences in the fecal microbiome will provide a foundation to improve our understanding the pathogenesis of PD and to support the potentially therapeutic options modifying the gut microbiota.

No abstract

Recent studies reported an association between gut microbiota composition and Parkinson’s disease (PD). However, we know little about the relationship between microbiome dysbiosis and the pathogenesis of PD. The objective of this study was to describe the evolution of fecal microbiota using an oral rotenone model of PD from a longitudinal study over a period of 4 weeks. Gastrointestinal function was assessed by measuring fecal pellet output, motor functions was assessed by open-field and pole tests every week. α-synuclein pathology, inflammation and tyrosine hydroxylase (TH) neuron loss from the middle brain were also analyzed. Fecal samples were collected every week followed by 16S rRNA sequencing and bioinformatics analysis. We reported that chronically oral administered rotenone caused gastrointestinal dysfunction and microbiome dysbiosis prior to motor dysfunction and central nervous system (CNS) pathology. 16S rRNA sequencing of fecal microbiome showed rotenone-treated mice exhibited fecal microbiota dysbiosis characterized by an overall decrease in bacterial diversity and a significant change of microbiota composition, notably members of the phyla Firmicutes and Bacteroidetes, with an increase in Firmicutes/Bacteroidetes ratio after 3 weeks of rotenone treatment. Moreover, rotenone-induced gastrointestinal and motor dysfunctions were observed to be robustly correlated with changes in the composition of fecal microbiota. Our results demonstrated that gut microbiome perturbation might contribute to rotenone toxicity in the initiation of PD and brought a new insight in the pathogenesis of PD. Novel therapeutic options aimed at modifying the gut microbiota composition might postpone the onset and following cascade of neurodegeneration.

Identification of the gut microbiome compositions associated with disease has become a research focus worldwide. Emerging evidence has revealed the presence of gut microbiota dysbiosis in Parkinson’s disease. In this study, we aimed to identify the gut microbiome associated with Parkinson’s disease and subsequently to screen and to validate potential diagnostic biomarkers of Parkinson’s disease. This case-control study investigated gut microbial genes in faeces from 40 volunteer Chinese patients with Parkinson’s disease and their healthy spouses using shotgun metagenomic sequencing. Furthermore, the identified specific gut microbial gene markers were validated with real-time PCR in an independent Chinese cohort of 78 Parkinson’s disease patients, 75 control subjects, 40 patients with multiple system atrophy and 25 patients with Alzheimer’s disease. We developed the first gut microbial gene catalogue associated with Parkinson’s disease. Twenty-five gene markers were identified that distinguished Parkinson’s disease patients from healthy control subjects, achieving an area under the receiver operating characteristic curve (AUC) of 0.896 (95% confidence interval: 83.1–96.1%). A highly accurate Parkinson’s disease index, which was not influenced by disease severity or Parkinson’s disease medications, was created. Testing these gene markers using quantitative PCR distinguished Parkinson’s disease patients from healthy controls not only in the 40 couples (AUC = 0.922, 95% confidence interval: 86.4–98.0%), but also in an independent group of 78 patients with Parkinson’s disease and 75 healthy control subjects (AUC = 0.905, 95% confidence interval: 86.0–95.1%). This classifier also performed a differential diagnosis power in discriminating these 78 patients with Parkinson’s disease from a cohort of 40 patients with multiple system atrophy and 25 patients with Alzheimer’s disease based on the panel of 25 biomarkers. Based on our results, the identified Parkinson’s disease index based on the gene set from the gut microbiome may be a potential diagnostic biomarker of Parkinson’s disease.

Magnetic reconnection is an important phenomenon extensively existing in the interplanetary space and planetary magnetosphere, such as solar flares, solar and stellar coronae, solar wind, planetary magnetosphere, the interplanetary space, the interstellar medium, neutron start, accretion disks, astrophysical jets, galaxy clusters, and black holes. The traditional cognition is that the energy carried by the magnetic field comes to explosions through reconnection. Ultimately the energy converts to the particles'kinetic and thermal energy, resulting in the acceleration and heating of the ions and electrons (e.g.,

The nature of the plasma wave modes around the ion kinetic scales in highly Alfvénic slow solar wind turbulence is investigated using data from the NASA's Parker Solar Probe taken in the inner heliosphere, at 0.18 Astronomical Unit (AU) from the sun. The joint distribution of the normalized reduced magnetic helicity σm (θRB, τ) is obtained, where θRB is the angle between the local mean magnetic field and the radial direction and τ is the temporal scale.Two populations around ion scales are identified: the first population has σm (θRB, τ) <0 for frequencies (in the spacecraft frame) ranging from 2.1 to 26 Hz for 60º < θRB < 130º, corresponding to kinetic Alfvén waves (KAWs), and the second population has σm (θRB, τ) >0 in the frequency range [1.4, 4.9] Hz for θRB > 150º, corresponding to Alfvén ion Cyclotron Waves (ACWs). This demonstrates for the first time the co-existence of KAWs and ACWs in the slow solar wind in the inner heliosphere, which contrasts with previous observations in the slow solar wind at 1 AU. This discrepancy between 0.18 and 1 AU could be explained, either by i) a dissipation of ACWs via cyclotron resonance during their outward journey, or by ii) the high Alfvénicity of the slow solar wind at 0.18AU that may be favorable for the excitation of ACWs.

Emerging evidence suggests that the microbiota present in feces plays a role in Parkinson’s disease (PD). However, the alterations of the microbiome in the blood of PD patients remain unknown. To test this hypothesis, we conducted this case-control study to explore the microbiota compositions in the blood of Chinese PD patients. Microbiota communities in the blood of 45 patients and their healthy spouses were investigated using high-throughput Illumina HiSeq sequencing targeting the V3-V4 region of 16S ribosomal RNA (rRNA) gene. The relationships between the microbiota in the blood and PD clinical characteristics were analyzed. No difference was detected in the structure and richness between PD patients and healthy controls. The following genera were enriched in the blood of PD patients: Isoptericola, Cloacibacterium, Enhydrobacter and Microbacterium; whereas genus Limnobacter was enriched in the healthy controls after adjusting for age, gender, body mass index (BMI) and constipation. Additionally, the findings regarding these genera were validated in another independent group of 58 PD patients and 57 healthy controls using real-time PCR targeting genus-specific 16S rRNA genes. Furthermore, not only the genera Cloacibacterium and Isoptericola (which were identified as enriched in PD patients) but also the genera Paludibacter and Saccharofermentans were positively associated with disease duration. Some specific genera in the blood were related to mood disorders. We believe this is the first report to provide direct evidence to support the hypothesis that the identified microbiota in the blood are associated with PD. Additionally, some microbiota in the blood are closely associated with the clinical characteristics of PD. Elucidating these differences in blood microbiomes will provide a foundation to improve our understanding of the role of microbiota in the pathogenesis of PD.

A BS TRACT: Background: Short-chain fatty acids (SCFAs) produced by gut microbiota are reduced in feces but paradoxically increased in plasma of patients with Parkinson's disease (PD), which may stem from intestinal wall leakage. Gut function should be taken into consideration when conducting microbial-metabolite research. Objective: The objective was to investigate synchronous changes of SCFAs in feces and plasma of patients with PD, taking constipation as a confounder to better disentangle the SCFA metabolism exclusively associated with PD. Methods: The concentrations of fecal and plasma SCFAs in 33 healthy control subjects and 95 patients with PD were measured using liquid and gas chromatography mass spectrometry, respectively. Patients with PD were divided into patients with PD without constipation (n = 35) and patients with PD with constipation (n = 60). Gut-blood barrier (GBB) permeability was assessed by plasma/fecal ratio of SCFA concentrations and fecal α1-antitrypsin concentration. Results: Patients with PD displayed decreased concentrations of fecal acetic, propionic, and butyric acid and increased concentrations of plasma acetic and propionic acid. Fecal acetic, isobutyric, and isovaleric acid were lower and plasma acetic and propionic acid were higher in patients with PD with constipation than in patients with PD without constipation. Constipation aggravated GBB permeability in patients with PD. Combined fecal and plasma SCFAs could discriminate patients with PD from healthy control subjects. Fecal SCFAs, except propionic acid, were negatively correlated with disease severity, while plasma acetic, propionic, and valeric acid showed a positive correlation. Conclusions: Our study showed alterations of fecal and plasma SCFAs in patients with PD that were associated with an impaired GBB and might be aggravated by constipation.