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Objective: To identify the impact of a collaborative pharmaceutical care service (CPCS) on medication safety and establish the impact of the CPCS on patient reported outcomes for Parkinson's disease (PD) patients. Methods: Initially, PD outpatients receiving the CPCS between March 2017 and March 2019 were compared with PD patients receiving standard of care to identify differences in management. Pharmacist interventions data were coded and patients with PD receiving the CPCS were compared with those receiving standard of care to determine differences in medicines prescribed and dosage associated with these. Following this, data of patients receiving CPCS at baseline and 3-months follow-up were collected using a questionnaire consisting of validated measures of two patient-reported outcomes [adherence and quality of life (QoL)]. Mean scores for continuous variables were calculated, with descriptive analysis of categorical variables consisting of frequency counts and percentages. Change in adherence score before and after CPCS was investigated using a Wilcoxon sign rank sum test, spearman correlation analysis was used to correlate the changes in QoL before and after CPCS with the number of interventions, and p < 0.05 indicates that the difference is statistically significant. Results: A total of 331 PD outpatients received CPCS over 490 outpatient visits with an average age of 71.83 (±12.54). Five hundred and forty-five drug related problems were recorded as pharmacist interventions, of which most involved change to dosage (n = 226, 41.47%), adverse drug reactions (n = 135, 24.77%), and change in a medication (n = 102, 18.72%). Compared with those receiving standard of care, patients receiving CPCS were significantly less likely to have been prescribed pramipexole (18.52 versus 23.77%, p < 0.001) and more likely to have been prescribed amantadine (5.40 versus 3.70%, p = 0.02) and selegiline (17.36 versus 11.64%, p < 0.001). Lower dosages of levodopa/benserazide (0.51 ± 0.31 g versus 0.84 ± 0.37 g, p < 0.001), levodopa/carbidopa (0.33 ± 0.23 g versus 0.66 ± 0.47 g, p < 0.001), pramipexole (1.14 ± 1.63 mg versus 1.27 ± 0.69 mg, p = 0.01), and entacapone (130.00 ± 79.76 mg versus 173.09 ± 97.86 mg, p < 0.001) were also recorded. At baseline 119 PD outpatients with an average age of 69.98 (±9.90) were recruited for the longitudinal study. At 3-month follow-up, participants reported improvement in bodily pain subscale (baseline versus 3-months follow-up, 30.04 ± 22.21 versus 23.01 ± 20.98, p = 0.037) and medication adherence (6.19 ± 1.50 versus 6.72 ± 1.73, p = 0.014). Frequency of CPCS use was related to activity of daily living subscale (p = 0.047), the bodily pain subscale (p = 0.026), and medication adherence (p = 0.011). Total score of PDQ-39 was associated with patient education (p = 0.005) and usage and dosage combined with patient education (p = 0.006), while medication adherence score was associated with usage and dosage (p = 0.005). Conclusion: The CPCS was effective in resolving drug-related problems and in improving patients' medication regimens, medication adherence, and QoL through patient education and dosage adjustments. This is the first step in the development and feasibility testing of pharmacy services for PD patients in China. [ABSTRACT FROM AUTHOR]

Researchers in China have developed a functional nucleic acid-based responsive artificial enzyme that enables continuous production of levodopa in a mouse model of Parkinson disease. [ABSTRACT FROM AUTHOR]

Mitochondrial abnormalities and a defective expression of neurotrophic factors contribute to neuronal damage in Huntington's disease (HD). HD patients showed a reduction in transforming growth factor-β1 (TGF-β1) levels in the peripheral blood and in cortical neurons. 3-n-butylphthalide (NBP) is first isolated from the seeds of celery, treats ischemic stroke in China. NBP could attenuate cognitive and motor impairments in the experimental models of Parkinson's disease and Alzheimer's disease, reduce mitochondrial oxidative stress and increase the expression of TGF-β1 in rats with focal cerebral ischemia. To our knowledge, the effect of NBP on Huntington's disease has not been reported. We proposed the hypothesis that whether NBP could protect mitochondria and regulate TGF-β1 and its downstream signaling in a HD animal model, further prevents motor dysfunction. Malonic acid is a reversible inhibitor of mitochondrial enzyme complex-II, induces energy crisis and free radical generation. In this study, we used intrastriatal injections of malonic acid in rats to mimic mitochondrial abnormalities and the other HD like symptoms. We found that treatment with NBP significantly attenuated malonic acid-induced motor and cognitive dysfunction in locomotor behaviour test, rotarod test, novel object recognition test and morris water maze test, prevented neurotoxicity and mitochondrial damage, activated TGF-β1/Akt/Wnt/β-Catenin pathway in striatum, but didn't regulate mitochondrial fusion and fission. The above effect was partly reversed by a PI3K/Akt inhibitor. Our data support NBP as a potential candidate for the treatment of HD. [ABSTRACT FROM AUTHOR]