ABSTRACT
AIM: To measure the concentration of glutamate in the serum of patients with Parkinson's disease (PD) and determine its association with clinical variants of disease course. MATERIAL AND METHODS: One hundred and ten patients with PD and 90 healthy people were examined. Glutamate concentration in the blood serum was determined with a spectrophotometric method. RESULTS AND CONCLUSION: Patients with Parkinson's disease had significantly higher levels of serum glutamate compared with healthy subjects (p<0,0001). Patients with a tremor-dominant subtype had significantly higher levels of serum glutamate compared to those in patients with akinetic-rigid and mixed subtypes. The results obtained allow us to expand our understanding of the pathogenesis of this disease. Changes in the concentration of glutamate may reflect neurodegenerative process in PD.
Subject(s)
Parkinson Disease , Disease Progression , Glutamic Acid , Humans , TremorABSTRACT
Clinical variants of Parkinson's disease (PD) are not restricted to motor symptoms but include a wide spectrum of different non-motor symptoms: cognitive, psychotic, autonomic and sensory. These non-motor symptoms often occur long before classical motor features. Associated pathologic changes can now be identified at earliest stages using neuroimaging, pathomorphological and genetic studies. Therefore, PD is currently considered as a multifactorial, heterogenic systemic disease associated with involvement of multiple neurotransmitter systems. This leads to understanding that not only dopaminergic but also other neurotransmitter systems, including glutamatergic system, are involved in the pathogenesis of PD. This article aimed at investigating a role of glutamatergic system in the initiation of neurodegenerative process. The role of glutamate as a neurotransmitter and a neurotoxin in the pathogenesis of PD and progression of its clinical manifestations is discussed. The authors suggest that research into glutamate excitotoxicity in PD patients might allow the improvement of treatment tactics and correction of pathogenetic therapy.
Subject(s)
Parkinson Disease , Dopamine , Glutamic Acid , Humans , Neurotransmitter AgentsABSTRACT
Microbiota is a community of microorganisms, viruses, protozoa, colonizing the gut. There are tight phylogenetic relationships between the gut microbiota and the human body, the disturbance of which may lead to the CNS dysfunction as well as to the development of neurodegenerative diseases. This review focuses on general and specific aspects of the influence of gut microbiota on the pathogenesis of Parkinson's disease (PD). Current theories and models of the relationship between microbiota and brain structures in PD are presented with a specific focus on neurochemical and immunological aspects of the problem.
Subject(s)
Gastrointestinal Microbiome , Parkinson Disease/microbiology , Brain , Gastrointestinal Tract , Humans , Microbiota , PhylogenyABSTRACT
Background: Despite the efforts of scientific community the data available on the correlation between emotional-affective symptoms of Parkinson's disease and changes in microbiome is still scarce. Deeper studies of nonmotor symptoms evident in premotor stages of the disease and the reciprocal influence of microbiota may help to understand the etiology and pathogenesis of PD neurodegeneration better. Aim of the Study: Discover the relations between emotional-affective disorders prevalent in PD population and changes in gut microbiota composition. Methods: 51 patient diagnosed with PD participated in the study. Every participant's emotional-affective state was examined using Beck's Depression Inventory (BDI) and Hospital Anxiety and Depression Scale (HADS). Taxonomic richness of microbiome was studied using 16S ribosomal RNA gene sequencing, bioinformatics, and statistical analysis. Results: Anxiety and depression are prevalent affective disorders in patients with PD. In our study, most of the subjects demonstrated certain anxiety and depression. Taxonomic diversity of gut microbiota in BP was increasing with the increase in anxiety levels, reaching the maximum in the group with subclinical anxiety, and decreasing in the group with clinically significant anxiety disorder. At the species level, patients with clinically significant anxiety had higher abundance of Clostridium clariflavum compared to the anxiety-free patients. Patients with moderate depression were characterized by the higher prevalence of Christensenella minuta, Clostridium disporicum, and Oscillibacter valericigenes compared to subjects without depression or with mild depression. Conclusion: The data we received in our study allow better understanding of PD pathogenesis.
