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Background IPX066 (Rytary®; carbidopa and levodopa [CD-LD] extended-release capsules) was designed to achieve therapeutic LD plasma concentrations within 1 h of dosing and maintain LD concentrations for a prolonged duration in early or advanced Parkinson's disease (PD). Methods In this open-label study, patients underwent 6 weeks of conversion to IPX066 from their prior controlled-release (CR) ± immediate-release (IR) CD-LD therapy and 6 months of maintenance (with an additional 6 months of IPX066 at some sites). Clinical utility was assessed at both the end of conversion and maintenance. Results Among 43 patients initiated on IPX066, 33 completed conversion. The mean LD conversion ratio was 1.8 among 30 patients previously on CR plus IR (and 1.5 among 3 previously taking CR alone). The mean IPX066 dosing frequency was 3.5 times/day compared with 2.6 times/day for CR plus 4.6 times/day for IR previously (and 4.7 times/day for CR alone). By patient and clinician global improvement ratings after 6-month maintenance, ≥ 43.8% of patients were much or very much improved from their previous treatment, and ≥ 68.8% were at least minimally improved. Adverse events were consistent with those reported in prior IPX066 studies. Conclusions These results suggest that advanced PD patients using CR CD-LD ± IR can be safely converted to IPX066, with high likelihood of achieving a stable regimen, less frequent LD dosing, and improved overall clinical benefit. Trial registration: Clinicaltrials.gov NCT01411137 .

Purpose The goal of the present study was to clarify the clinical characteristics and laboratory results of parkinsonian symptoms among patients with and without camptocormia. Methods Seventy-eight Parkinson's disease (PD) patients with camptocormia and 78 PD patients without camptocormia underwent a neurological examination, a blood test, and spinal magnetic resonance imaging (MRI). PD with camptocormia group and PD with non-camptocormia group were matched on age, age at PD onset, and sex. Principal results Camptocormia group had significantly higher prevalence of compression fractures, more severe parkinsonian symptoms, and a greater incidence of dementia than those without camptocormia. Serum creatine kinase levels in camptocormia group significantly elevated compared with non-camptocormia group. There were higher prevalence of abnormal findings in spine MRI including compression fractures and paravertebral muscle changes in camptocormia group compared with non-camptocormia group. Major conclusions Camptocormia is associated with a greater prevalence of compression fractures and associated with greater UPDRS part II, part III score, axial score, and lower MMSE in this cross-sectional study. Thus, it can be concluded that camptocormia in PD is predominantly myopathic.

To investigate the impact of non-motor symptoms on health-related and perceived quality of life in Parkinson's disease (PD).One hundred and fifty PD patients (57.3% males; 70.9±8.6years old) were included in this cross-sectional, monocenter, evaluation study. Multiple linear regression methods were used to evaluate the direct impact of non-motor symptoms (as assessed by the Non-Motor Symptoms Scale [NMSS]) on 1) the 39-item PD Quality of Life Questionnaire Summary Index score (PDQ-39SI), and 2) a subjective assessment of perceived quality of life (PQ-10), after adjusting for age, sex, mood (Beck Depression Inventory), disability (SchwabEngland Activities of Daily Living Scale), and PD-specific motor dysfunction (ON-state HoehnYahr/Unified Parkinson's Disease Rating Scale [UPDRS] part III, and motor complications [UPDRS part IV]).Higher NMSS total scores were systematically associated with worse quality of life (for PDQ-39SI, p=0.013; for PQ-10, p=0.017). PD-specific motor dysfunction had a larger negative impact on health-related quality of life (PDQ-39SI) than non-motor symptoms (2.8% vs 0.7%). In contrast, the negative impact of non-motor symptoms on perceived quality of life (PQ-10) was larger than that found for PD-specific motor dysfunction (2.8% vs 0.9%). While the model for PDQ-39SI provided an adequate fit (adjusted R-squared, 0.83), a substantial proportion of the PQ-10 variance remained unexplained (adjusted R-squared, 0.48).Non-motor symptoms have a direct negative impact on health-related and perceived quality of life in PD. Perceived quality of life is not adequately explained by motor and non-motor manifestations of the disease.

To study what comorbid conditions were present at baseline and 3years later in a cohort of Spanish Parkinson's disease (PD) patients, to compare comorbidity with both Alzheimer's disease (AD) and control groups and to analyze the role of comorbidity as predictor of mortality.One hundred and forty-seven non-demented PD patients (57.1% males; 70.9±8.6years old) were included in this 36months follow-up (2012-2015), monocenter, evaluation study. The International Classification of Diseases, Tenth Revision (ICD-10), Charlson Index (CI), Comorbidity-Polypharmacy Score (CPS) and Elixhauser Comorbidity Measure (ECM) were used to assess comorbidity at baseline and at 3years. Forty-four AD patients and 44 control subjects were included as comparator groups.Total number of comorbidities (ICD-10) and polypharmacy at baseline were higher in PD and AD patients than controls (4.4±2.3 vs 5.2±2.4 vs 3.4±1.9 [p=0.001] and 81.6% vs 75% vs 56.8% [p=0.003], respectively). Diseases of the circulatory system (ICD-10/chapter-IX) and endocrine, nutritional and metabolic diseases (ICD-10/chapter-IV) were the most frequent in all groups. There was a significant increase in comorbidity (mean, +1.6±2.8) in all groups (p0.0001) without differences between them. Seventeen patients died and 8 cases were did not follow-up. Comorbidity was a predictor of death in PD patients after adjust for other covariates (including age, sex, disease duration, disease stage, motor status and non-motor symptoms): ICD-10 (total number of comorbidities), hazard ratio 1.285 (95% confidence interval, 1.047-1.577; p=0.017); CI, hazard ratio 1.462 (95% confidence interval, 1.045-2.047; p=0.027).Comorbidity is frequent in PD patients, increases significantly over time and predicts mortality.

Background Parkinson's disease (PD) is an oxidative stress-mediated degenerative disorder. Elevated plasma homocysteine (Hcy) is frequently found in the levodopa-treated PD patients, is associated with disease progression and is a marker of oxidative stress. Whey protein is a rich source of cysteine, and branched-chain amino acids (BCAA). It has been shown that supplementation with Whey protein increases glutathione synthesis and muscle strength. Objectives and methods In this study, we conducted a placebo-controlled, double-blind study (NCT01662414) to investigate the effects of undenatured Whey protein isolate supplementation for 6 months on plasma glutathione, plasma amino acids, and plasma Hcy in PD patients. Clinical outcome assessments included the unified Parkinson's disease rating scale (UPDRS) and striatal L-3,4-dihydroxy-6-(18)F-fluorophenylalanine (FDOPA) uptake were determined before and after supplementation. 15 patients received Whey protein, and 17 received Soy protein, served as a control group. Results Significant increases in plasma concentration of reduced glutathione and the ratio of reduced to oxidized glutathione were found in the Whey-supplemented patients but not in a control group. This was associated with a significant decrease of plasma levels of Hcy. The plasma levels of total glutathione were not significantly changed in either group. Plasma BCAA and essential amino acids (EAA) were significantly increased in the Whey-supplemented group only. The UPDRS and striatal FDOPA uptake in PD patients were not significantly ameliorated in either group. However, significant negative correlation was observed between the UPDRS and plasma BCAA and EAA in the pre-supplemented PD patients. Conclusion This study is the first to report that Whey protein supplementation significantly increases plasma reduced glutathione, the reduced to oxidized glutathione ratio, BCAAs and EAAs in patients with PD, together with a concomitant significant reduction of plasma Hcy. However, there were no significant changes in clinical outcomes. Long-term, large randomized clinical studies are needed to explore the benefits of Whey protein supplementation in the management of PD patients.

Parkinson's disease (PD) is a neurodegenerative disorder, characterised by the progressive loss of dopaminergic neurons in the substantia nigra, and typically treated by dopamine replacement. This treatment, although very effective in the early stages of the disease, is not curative and has side-effects. As such there has been a search for a more definitive treatment for this condition, which has mainly concentrated on replacing the lost neurons with neural grafts. Possible cell sources for replacement range from autologous grafts of dopamine secreting cells to allografts of fetal ventral mesencephalon and neural precursor cells derived from fetal tissue or embryonic stem cells. Some of these cells have been the subject of clinical trials, which to date have produced disparate outcomes. Therefore, whilst cell therapies remain a promising treatment for PD, there is need for further refinement of the techniques involved in this experimental procedure, before any new trials in patients are undertaken.