Gut microbiota, which act as a determinant of pharmacokinetics, have long been overlooked. In recent years, a growing body of evidence indicates that the gut microbiota influence drug metabolism and efficacy. Conversely, drugs also exert a substantial influence on the function and composition of the gut microbiota. Pharmacomicrobiomics, an emerging field focusing on the interplay of drugs and gut microbiota, provides a potential foundation for making certain advances in personalized medicine. Understanding the communication between gut microbiota and antiparkinsonian drugs is critical for precise treatment of Parkinson's disease. Here, we provide a historical overview of the interplay between gut microbiota and antiparkinsonian drugs. Moreover, we discuss potential mechanistic insights into the complex associations between gut microbiota and drug metabolism. In addition, we also draw attention to microbiota-based biomarkers for predicting antiparkinsonian drug efficacy and examine current state-of-the-art knowledge of microbiota-based strategies to optimize drug therapy in Parkinson's disease.

Previous studies have shown that Helicobacter pylori infection is not only a risk factor for gastrointestinal diseases but also associated with various non-digestive conditions. This study aimed to investigate the effect of Helicobacter pylori infection on the risk of lipid metabolism disorders and cardiovascular disease in individuals with diabetes mellitus.

This cross-sectional study was conducted at a health examination center. Data from life questionnaires, laboratory tests, the carbon-13 urea breath test, and the Framingham Risk Score were collected from 266 patients with diabetes. All participants were categorized into Helicobacter pylori-uninfected and Helicobacter pylori-infected groups based on the carbon-13 urea breath test results. Differences in lipid levels, Framingham Risk Score, and cardiovascular disease risk were compared between the two groups. A logistic regression model was applied to analyze whether Helicobacter pylori infection is an independent risk factor for dyslipidemia in patients with diabetes.

Total cholesterol and low-density lipoprotein cholesterol levels were higher in the Helicobacter pylori-infected group than in the uninfected group, and high-density lipoprotein cholesterol levels were lower in the infected group (both P <  0.05). There was no statistically significant difference in triglyceride levels between the two groups. Regression analysis showed that Helicobacter pylori infection was an independent risk factor for dyslipidemia in patients with diabetes (P <  0.05). The Framingham Risk Score and 10-year cardiovascular disease risk were higher in the Helicobacter pylori-infected group compared with the uninfected group (P <  0.001).

Helicobacter pylori infection is associated with dyslipidemia and may contribute to an increased risk of cardiovascular disease in individuals with diabetes.

The human gut microbiota is diverse and abundant and plays important roles in regulating health by participating in metabolism and controlling physiological activities. The gut microbiota and its metabolites have been shown to affect the functioning of the gut and central nervous system through the microbiota-gut-brain axis. It is well established that microbiota play significant roles in the pathogenesis and progression of Parkinson's disease (PD). Disorders of the intestinal microbiota and altered metabolite levels are closely associated with PD. Here, the changes in intestinal microbiota and effects of metabolites in patients with PD are reviewed. Potential mechanisms underlying intestinal microbiota disorders in the pathogenesis of PD are briefly discussed. Additionally, we outline the current strategies for the treatment of PD that target the gut microbiota, emphasizing the development of promising novel strategies.

Helicobacter pylori (H. pylori) infection affects around half of the global population and is a globally highly prevalent pathogen that is closely linked not only to gastrointestinal diseases such as chronic atrophic gastritis, functional dyspepsia and peptic ulcer but also to the development and progression of a variety of extra-gastrointestinal diseases. Numerous studies have shown the correlation between H. pylori infection and iron-deficiency anemia (IDA). The prevalence of H. pylori infection is higher in individuals with IDA, and the hemoglobin level of patients with IDA can be increased to different degrees or even returned to normal following active H. pylori eradication. However, this conclusion is still controversial. In this paper, a comprehensive literature search was conducted using the PubMed/MEDLINE/Web of Science database, combining the following terms: "Helicobacter pylori," "Helicobacter pylori infection," "iron deficiency anemia," "iron deficiency," "iron absorption," "iron malabsorption," "serum iron," "hemoglobin," "pathogenesis," "mechanism," and "eradication therapy." Through extensive literature searches, the correlation between H. pylori infection and IDA, its potential mechanism, and the efficacy of H. pylori eradication therapy in IDA patients have been comprehensively discussed. We conclude that the majority of existing studies have confirmed the correlation between H. pylori infection and IDA, indicating that patients with H. pylori infection are more likely to develop IDA and that the prevalence of H. pylori infection is higher in individuals with IDA. Compared with iron supplementation alone, combining H. pylori eradication with iron supplementation is more effective in treating IDA, particularly in unexplained or refractory IDA cases. These findings provide valuable insights for clinicians managing patients with unexplained or refractory IDA.

Changes in population demographics indicate that the elderly population will reach 2.1 billion worldwide by 2050. In parallel, there will be an increase in neurodegenerative diseases such as Alzheimer's and Parkinson's. This review explores dysbiosis occurring in these pathologies and how virulence factors contribute to the worsening or development of clinical conditions, and it summarizes existing and potential ways to combat microorganisms related to these diseases. Microbiota imbalances can contribute to the progression of neurodegenerative diseases by increasing intestinal permeability, exchanging information through innervation, and even acting as a Trojan horse affecting immune cells. The microorganisms of the microbiota produce virulence factors to protect themselves from host defenses, many of which contribute to neurodegenerative diseases. These virulence factors are expressed according to the genetic composition of each microorganism, leading to a wide range of factors to be considered. Among the main virulence factors are LPS, urease, curli proteins, amyloidogenic proteins, VacA, and CagA. These factors can also be packed into bacterial outer membrane vesicles, which transport proteins, RNA, and DNA, enabling distal communication that impacts various diseases, including Alzheimer's and Parkinson's.

In this hypothesis article, the potential clinicopathological associations of Calcitonin Gene Related Peptide (CGRP) with the development of synuclein-associated neurodegenerative disorders (SAND) are discussed. The presence of α-syn and CGRP in the CNS and the ENS and the intricate role of CGRP and its related pathways in inflammation, apoptosis, metabolism, neuromodulation, and brain-gut communication are analyzed. Since this hypothesis is confirmed, modulating CGRP-potential related pathways may lead to novel disease-modifying therapies.

Constipation is one of the most common nonmotor symptoms (NMSs) of Parkinson's disease (PD). The infection rate of Helicobacter pylori (HP) is greater in PD patients. This study was a multicenter prospective cohort study in which propensity score matching (PSM) was used to determine whether HP infection was a risk factor for constipation in patients with PD.

A total of 932 PD patients with 13C-urea breath test for HP were included in the study. The PSM was estimated with the use of a nonparsimonious multivariate logistic regression model, with HP infection as the dependent variable and all the baseline characteristics as covariates. A total of 697 patients composed the study cohort, including 252 (36.2 %) patients in the HP-positive (HPP) group and 445 (63.8 %) patients in the HP-negative (HPN) group. Before PSM, there were differences in several of the baseline variables between the two groups. After PSM, 250 HPP patients were matched with 250 HPN patients and the standardized differences were less than 0.1 for all variables.

The present results demonstrate that HP infection is a risk factor for constipation in patients with PD [RR (95 % CI) 1.412 (1.155-1.727), P < 0.001]. Subgroup analyses revealed that HP infection was both a risk factor for constipation in Hoehn-Yahr scale (1,1.5) group and Hoehn-Yahr scale (2-5) group [OR (95 % CI) 1.811 (1.079-3.038), P < 0.025; OR (95 % CI) 2.041 (1.177-3.541), P < 0.011].

The results of our prospective cohort study suggest that Helicobacter pylori infection is a risk factor for constipation in patients with PD.

ChiCTR2300071631.

Increasing evidence suggests an association between Helicobacter pylori (HP) infection and Parkinson's disease (PD) and its clinical manifestations, but the causal relationship remain largely unknown.

To investigate the causal relationship between HP infection and PD risk, PD symptoms, and secondary parkinsonism, we conducted two-sample Mendelian randomization (MR).

We obtained summary data from genome-wide association studies for seven different antibodies specific to HP proteins and five PD-related phenotypes. The inverse-variance weighted (IVW), weighted median, weighted mode, and MR-Egger methods were used to assess the causal relationships. Sensitivity analyses were performed to examine the stability of the MR results and reverse MR analysis was conducted to evaluate the presence of reverse causality.

Genetically predicted HP antibodies were not causally associated with an increased risk of PD. However, HP cytotoxin-associated gene-A (CagA) and outer membrane protein (OMP) antibody level were causally associated with PD motor subtype (tremor to postural instability/gait difficulty score ratio; β = -0.16 and 0.46, P = 0.002 and 0.048, respectively). HP vacuolating cytotoxin-A (VacA) antibody level was causally associated with an increased risk of PD dementia [odds ratio (OR) = 1.93, P = 0.040]. Additionally, HP OMP antibody level was identified as a risk factor for drug-induced secondary parkinsonism (OR = 2.08, P = 0.033). These results were stable, showed no evidence of heterogeneity or directional pleiotropy, and no evidence of a reverse causal relationship.

Our findings indicate that HP infection does not increase the risk of PD, but contributes to PD motor and cognitive symptoms. Different types of HP antibodies affect different symptoms of PD. Eradication of HP infection may help modulate and improve symptoms in PD patients.

Parkinson's disease (PD) is viewed as a progressively deteriorating neurodegenerative disorder, the exact etiology of which remains not fully deciphered to this date. The gut microbiota could play a crucial role in PD development by modulating the human immune system.

This study aims to explore the relationship between gut microbiota and PD, focusing on how immune characteristics may both directly and indirectly influence their interaction.

Utilizing cumulative data from genome-wide association studies (GWAS), our research conducted a two-sample Mendelian randomization (MR) analysis to clarify the association between the gut microbiome and PD. Additionally, by employing a two-step MR approach, we assessed the impact of gut microbiota on PD development via immune characteristics and quantified HLA-DR mediation effect on plasmacytoid dendritic cells (pDCs).

We discovered significant associations between PD and microbiota, comprising one class, one order, two families, and two genera. Furthermore, we explored the extent to which HLA-DR on pDCs mediates the effect of Butyrivibrio gut microbiota on PD.

Our study emphasizes the complex interactions between the gut microbiota, immune characteristics, and PD. The relationships and intermediary roles identified in our research provide important insights for developing potential therapies that target the gut microbiome to alleviate symptoms in PD patients.