Thus, clinical features of non-motor symptoms were described both in carriers of GBA mutations and polymorphisms. Identification of the specific clinical phenotype of PD in carriers of GBA polymorphic variants is important due to their relatively high prevalence in PD patients.
Parkinson’s disease (PD) is a neurodegenerative disease characterized by α-synucleinopathy, which involves all districts of the brain-gut axis, including the central, autonomic and enteric nervous systems. Previous findings suggest that the intestinal microbiome is altered in PD and is related to motor phenotype. However how dysbiosis arises and whether this feature contributes to PD pathogenesis remains unknown. The aim was to evaluate gut microbiome and the serum cytokine profile in PD. We quantified serum interleukin (IL) levels (IL-1β, IL-6, IL-10, TNF-α, IFN-γ) in 55 PD patients. Study of the fecal samples was performed by real time PCR method and bacteriologically. Discovered the relationship between the intensity of dysbiosis and the level of proinflammatory cytokine IFN-γ, IL-6.We show that disturbances in plasma cytokine level could be more profound in PD patients with altered composition of intestinal microbiota, which may explain the mechanism of influence of microbiota composition on the PD manifestations.
The article reviews the causes of gait impairment in patients with Parkinson's disease (PD). The emphasis is made on modern ideas, according to which gait impairment in PD is caused by a multisystem lesion and non-dopaminergic dependent mechanisms play the leading role. It is highlighted that gait impairment in PD is associated with the disruption of frontal/subcortical neural pathways which requires a special approach to pharmacological and non-pharmacological therapy. Based on pathogenetic mechanisms, much attention is paid to anti-dementia medications. Attention is drawn to the fact that the use of memantine hydrochloride (akatinol memantine) is a promising direction for gait impairment correction in the advanced and late stages of PD due to the improvement of glutamatergic transfer from the striatum to the specific areas of the cerebral cortex involved in gait control. The results of the latest clinical trials are analyzed.
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