LCSB coordinates European project on Parkinson’s research

Look at that word 'coordination', something we don't have anywhere in stroke. You're screwed as a stroke survivor until the complete stroke leadership is replaced with stroke survivors.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=159042&CultureCode=en
The Luxembourg Centre for Systems Biomedicine (LCSB) of the University of Luxembourg is coordinating an EU project for research into new active compounds against Parkinson’s disease (PD). SysMedPD (Systems Medicine of Mitochondrial Parkinson’s Disease) is the name of the project that just started with the involvement of five universities and three companies from Luxembourg, Germany, Ireland, the Netherlands and UK. The European Union is funding the researchers of this consortium with a total of 5.9 million euros.
With this funding, they will be developing novel techniques by which to identify and research into active compounds against PD. They will furthermore be advancing drug candidates towards their medical application. “Universities and biopharmaceutical companies complement each other’s expertise ideally in SysMedPD,” says Prof. Rudi Balling, LCSB director and coordinator of SysMedPD. “This creates optimal conditions in which to progress a good deal further in developing diagnoses and therapies for Parkinson’s disease.”
Parkinson’s disease is a gradually progressive disease of human nerve tissue, resulting among other things in muscle tremors and muscle rigidity. The mitochondria of nerve cells are often causally involved in the onset – mitochondria being the power plants of cells, in which biochemical reactions provide energy for cellular metabolic processes. “We estimate that in about ten to twenty percent of all Parkinson’s patients, their mitochondria do not function properly,” says senior LCSB scientist Dr Ronan Fleming, who is significantly involved in the conception and coordination of SysMedPD. “In order to better diagnose, heal or at least effectively curb the progression of Parkinson’s disease, we must understand this dysfunction of mitochondria in detail.”
The researchers within SysMedPD are first concentrating on such patterns of PD in which the mitochondria are damaged by mutations in individual genes. “Later, the results can then be carried over to patient groups in which multiple genes and environmental factors are involved in the onset of PD,” adds Dr Fleming.
The SysMedPD consortium will tackle this task with different approaches: “At the LCSB, we place emphasis on developing new, computational models by which we can better depict the processes going on inside mitochondria,” Ronan Fleming says. Prof. Jens Schwamborn, head of the LCSB group Development and Cell Biology, describes a complementary approach: “We must verify any computational predictions using experiments. Therefore, in the scope of this EU project, we will also employ advanced cellular models, where skin samples obtained from Parkinson’s disease patients are reprogrammed into living human nerve cells.”
To ensure the research results obtained within SysMedPD are translated into application as quickly as possible, the consortium also has biopharmaceutical companies on board. Their areas of involvement are test development for new active compounds and identification of active compounds. “The project is organised such that the insights that we and the other academic partners gain will complement those of the companies involved very well,” says Prof. Rudi Balling. “With this close connection between public and private research, we can ensure the EU funding, firstly, is employed optimally in the interest of the PD patients and, secondly, will generate economic stimuli. These are important objectives of the EU that we will fulfil here.”
The SysMedPD partners:
-       Germany: University of Lübeck (Prof. Christine Klein), EURICE – European Research and Project Office GmbH (Corinna Hahn)
-       Ireland: Maynooth University (Dr Niall Finnerty)
-       Luxembourg: University of Luxembourg (Prof. Rudi Balling, Dr Ronan Fleming, Prof. Jens Schwamborn)
-       Netherlands: Leiden University (Prof. Thomas Hankemeier), Khondrion BV (Prof. Jan Smeitink), Mimetas BV (Dr Paul Vulto)
-       Great Britain: University College London (Prof. Anthony Schapira)
http://wwwen.uni.lu/university/news/latest_news/lcsb_coordinates_european_project_on_parkinson_s_disease_research

Impairment in task-specific modulation of muscle coordination correlates with the severity of hand impairment following stroke

Not sure how this could possibly help me. I have no individual finger control. I think I somehow need to stop the damnable finger spasticity first.
http://search.naric.com/research/rehab/redesign_record.cfm?search=2&type=all&criteria=J67539&phrase=no&rec=123308
NARIC Accession Number: J67539.  What's this?
Author(s): Lee, Sang W.; Triandafilou, Kristen; Lock, Blair A.; Kamper, Derek G..
Project Number: H133F090018.
Publication Year: 2013.
Number of Pages: 18.
Abstract: Study examined post-stroke impairment in the ability to modulate muscle coordination patterns across tasks and its correlation with hand impairment. Fourteen stroke survivors, divided into a group of 8 subjects with severe hand impairment and a group of 6 subjects with moderate hand impairment according to their clinical functionality score, participated in the experiment. Another four neurologically intact subjects participated in the experiment to serve as a point of comparison. Activation patterns of nine hand and wrist muscles were recorded using surface electromyography while the subjects performed six isometric tasks. Patterns of covariation in muscle activations across tasks, i.e., muscle modules, were extracted from the muscle activation data. Results showed that the degree of reduction in the inter-task separation of the multi-muscle activation patterns was indicative of the clinical functionality score of the subjects (mean value = 26.2 for severely impaired subjects, 38.1 for moderately impaired subjects). The number of muscle modules extracted from the muscle activation patterns of a subject across six tasks, which represents the degree of motor complexity, was found to be correlated with the clinical functionality score. Greater impairment was also associated with a change in the muscle module patterns themselves, with greater muscle coactivation. A substantial reduction in the degrees-of-freedom of the multi-muscle coordination poststroke was apparent, and the extent of the reduction, assessed by the stated metrics, was strongly associated with the level of clinical impairment.