A Case Report of Non-Motor Symptoms Evaluated Using the Non-Motor Symptom Scale in a Patient with Secondary Parkinsonism Presumed to be Probable Lewy Body Dementia and Improved with Combined Treatment with Herbal Medicine and Acupuncture

Parkinson's syndrome is a degenerative brain disease that presents characteristic motor symptoms of tremor, rigidity, and gait disturbance. In addition to these motor symptoms, Parkinson's syndrome also presents non-motor symptoms (NMSs) such as sleep disturbance and cognitive decline. NMSs reduce patient's quality of life and psychosocial functioning and cause economic burden on the patient, so appropriate evaluation and treatment are required. Lewy body dementia is one of the several diseases belonging to Parkinson's syndrome. Its symptoms such as cognitive function, memory impairment, and hallucinations occur with Parkinsonism. Although drug therapy is being used with drug treatment to treat non-motor symptoms, it has limitations such as side effects, which stimulated interest in other complementary treatment methods such as oriental medicine treatment, dance, and yoga. The patient in this case complained of tremor in the right upper extremity, muscle hypertension and pain, and persistent vision, memory, and cognitive decline. The patient was diagnosed with probable Lewy body dementia. The patient was hospitalized for 4 months and received acupuncture and herbal medicines. After treatment, the patient's NMS scale scores decreased from 90 to 63, and the Unified Parkinson's Disease Rating Scale scores (summed I, II, and III) decreased from 17 points to 8 points. The Beck Depression Inventory score decreased from 22 points to 13 points. In addition, the patient's subjective evaluation revealed improvement. In this case, a patient diagnosed with probable Lewy body dementia who did not respond to the standard treatment and did not want to take medications showed improvement in not only motor symptoms but also NMSs after integrative Korean medicine treatment.

Preparation of a Carboxymethyl Chitosan-Loaded L-Dopa Composite Nano-Pharmaceutical and Its Therapeutic Effect on Parkinson’s Syndrome

Parkinson’s syndrome (PD) is the second-most common neurodegenerative disease in the world. The chronic disability of PD and the long-term medication required to treat it imposes a huge economic burden on patients and society. Thus, enhancing the therapeutic effect of PD drugs while reducing the side effects caused by long-term drug use has become a challenge that researchers need to overcome. In this study, a compound drug—levodopa/carboxymethyl chitosan/resveratrol nanoparticles (LDP/CMCS/RVT NPs)—with both sustained release and neuroprotective effects was constructed based on carboxymethyl chitosan. The new LDP compound nano-drug can significantly promote glutathione levels of and superoxide dismutase in the substantia nigra and striatum of mice, while increasing the expression of the brain-derived neurotrophic factor. Based on these findings, LDP/CMCS/RVT NPs is expected to provide a new therapeutic strategy for the recovery of midbrain dopamine deficiency and neuroinflammatory changes in PD patients.

Machine Learning Techniques for Parkinson’s Disease Detection using Wearables during a Timed-up-and-Go-Test

In this paper, the classification models for Idiopathic Parkinson's syndrome (iPS) detection through timed-up-and-go test performed on iPS-patients are given. The models are based on the supervised learning. The data are extracted via Myo gesture armband worn on two hands. The corresponding models are based on extracted features from signal data and raw signal data respectively. The achieved accuracy from both models are 0.91 and 0.93 with reasonable specificity and sensitivity.

Functional activity of p-glycoprotein in blood-brain barrier during experimental par-kinson's syndrome

Background. P-glycoprotein (Pgp, ABCB1-protein) is a membrane transporter with broad substrate specificity that is localized in hepatocytes, enterocytes, epithelial renal tubules, and also in tissue barriers, including blood-brain barrier (BBB). Increased Pgp activity in BBB is one of the reasons for the pharmacoresistance of a number of CNS diseases. Aim. Analysis of Pgp functional activity in BBB during experimental Parkinson's syndrome. Materials and Methods. The work was performed on 90 Wistar rats, divided into 3 series (n=30 in each). The 1 series (control) was subcutaneously injected sunflower oil once a day for 7 days, and Pgp activity in BBB was assessed on the 8th day. The 2 and 3 series (pathology control) - were administered rotenone at a dose of 2.5 mg/kg once a day for 7 and 28 days respectively to simulate parkin-sonism. At the end of the experiment Pgp activity was estimated. To confirm Parkinson's syndrome, in addition to the clinical picture, level of dopamine in midbrain and striatum was determined using enzyme-linked immunosorbent assay. Pgp functional activity in BBB was assessed by the degree of penetration of its marker substrate fexofenadine into the brain after its intravenous administration at a dose of 10 mg/kg. The content of fexofenadine in the blood plasma and in brain tissue was estimated by the area under pharmacokinetic curve of the substance (in the blood or brain tissues) - AUC0-t(plasma) or AUC0-t(brain) respectively. To assess the BBB permeability the ratio AUC0-t(brain) / AUC0-t(plasma) was calculated. Results. Rotenone administration led to the development of parkinsonism typical picture: muscle stiffness, hypokinesia, gait instability. There was a decrease in dopamine level in the striatum after 7 days by 69.6% (p=0.095), after 28 days - by 93.9% (p=0.008), in midbrain - by 72.7% (p=0.095) and 68.7% (p=0.032) respectively. Fexofenadine AUC0-t(plasma) and AUC0-t(brain) after its intravenous administration to control rats were 266.2 (246.4; 285.6) μg/ml*min and 5.9 (5.8;6.6) µg/g*min respectively, AUC0-t(brain) /AUC0-t(plasma) - 0.020 (0.019; 0.022). When rotenone was for 7 days administered - fexofenadine AUC0-t(brain) increased 2.02 times (p=0.0163), AUC0-t(brain) / AUC0-t(plasma) - 2.4 times (p=0.0283). 28 days administration of rotenone led to augmentation of AUC0-t(brain) of fexofenadine by 1.75 times (p=0.0283), AUC0-t(brain) / AUC0-t(plasma) - by 2.27 times (p=0.0163). Conclusions. The development of Parkinson’s syndrome, caused by the administration of rotenone, inhibits Pgp functional activity in BBB, which is confirmed by the accumulation in the brain marker substrate of the transporter - fexofenadine.