Teamwork helps

An open access article:

Multi-disciplinary approach for rehab to improve QOL

From the abstract:

Results:Patients reported higher functional status (d=0.37,p<0.001), general self-efficacy(d=0.28,p<0.01), and quality of life (d=0.32,p<0.001) at three weeks follow-up, comparedto their baseline scores. The regression analysis showed that having a better initial functionalstatus (β=−0.26,p<0.05) and lower quality of life (β=0.51,p<0.001) were associated withmore improvements in quality of life.
Conclusion:The study suggests that actual functioning in persons with Parkinson’s diseaseis a better predictor of improved quality of life than self-efficacy beliefs and that those whohave lower levels of initial quality of life benefit more from rehabilitation.

The program was only three weeks long, but was inpatient and apparently intensive:

The multidisciplinary rehabilitation program had a duration of three weeks and was an inpatient program. Upon arrival, participants were awarded a primary contact to ensure a unified team working toward goals set by the participant him/herself. The multidisciplinary team consisted of 10 different professions, such as occupational therapists, physical therapists, doctors, neurologists, nurses, sports educators, cognitive behavioral therapists, and nutritionists. Commencing the multidisciplinary rehabilitation program, participants were assessed by the relevant professional/s and typically had close follow-up the first week with individual and group-based exercise

 

New approach – direct brain infusions to regrow dopaminergic neural cells

This approach might help, but apparently it will take about 18 months to get results in moderately advanced cases. (emphasis added to abstract below).

One wonders whether complementary therapeutic treatments (exercise, dance (movement + rhythm), singing, or music instrument training were being used by any of the participants, or whether this was the only treatment these subjects were using during this time. Certainly worth trying this in combination with other, non-invasive treatments (says the cyborg with electrodes stimulating the subthalamus nigra substantia).

Journal of Parkinson’s Disease research pre-press

Abstract.
Background: Intraputamenal glial cell line-derived neurotrophic factor (GDNF), administered every 4 weeks to patients with moderately advanced Parkinson’s disease, did not show significant clinical improvements against placebo at 40 weeks,
although it significantly increased [18F]DOPA uptake throughout the entire putamen.
Objective: This open-label extension study explored the effects of continued (prior GDNF patients) or new (prior placebo patients) exposure to GDNF for another 40 weeks.
Methods: Using the infusion protocol of the parent study, all patients received GDNF without disclosing prior treatment allocations (GDNF or placebo). The primary outcome was the percentage change from baseline to Week 80 in the OFF state
Unified Parkinson’s Disease Rating Scale (UPDRS) motor score.
Results: All 41 parent study participants were enrolled. The primary outcome decreased by 26.7 ± 20.7% in patients on GDNF for 80 weeks (GDNF/GDNF; N = 21) and 27.6 ± 23.6% in patients on placebo for 40 weeks followed by GDNF for 40 weeks
(placebo/GDNF, N = 20; least squares mean difference: 0.4%, 95% CI: –13.9, 14.6, p = 0.96). Secondary endpoints did not show significant differences between the groups at Week 80 either. Prespecified comparisons between GDNF/GDNF at Week 80 and placebo/GDNF at Week 40 showed significant differences for mean OFF state UPDRS motor (–9.6 ± 6.7 vs. –3.8 ± 4.2 points, p = 0.0108) and activities of daily living score (–6.9 ± 5.5 vs. –1.0 ± 3.7 points, p = 0.0003). No treatment-emergent safety concerns were identified.

Conclusions: The aggregate study results, from the parent and open-label extension suggest that future testing with GDNF will likely require an 80- rather than a 40-week randomized treatment period and/or a higher dose.

Might mitophagy be enlisted in the fight against Parkinson’s?

Mitochondrial dysfunction and Parkinson’s

During aging, the process of mitophagy, a system that allows the removal of dysfunctional mitochondria through lysosomal degradation, starts to malfunction. Because of this defect, damaged mitochondria are not removed correctly, and their decomposing components accumulate inside the cells. Dysfunctional mitochondria that are not removed by mitophagy produce high amounts of reactive oxygen species (ROS) and, thus, cause oxidative stress. Oxidative stress, in turn, is very harmful for the cells, neuronal cells, in particular. Consequently, the process of mitophagy plays a crucial role in mitochondria-related disease. Mitochondrial dysfunctions and oxidative stress are well-established factors contributing to Parkinson’s disease (PD), one of the most common neurodegenerative disorders. In this review, we report various known antioxidants for PD treatments and describe the stimulation of mitophagy process as a novel and exciting method for reducing oxidative stress in PD patients. We describe the different mechanisms responsible for mitochondria removal through the mitophagy process. In addition, we review the functional connection between mitophagy induction and reduction of oxidative stress in several in vitro models of PD and also agents (drugs and natural compounds) already known to be antioxidants and to be able to activate mitophagy. Finally, we propose that there is an urgent need to test the use of mitophagy-inducing antioxidants in order to fight PD.