Proposals sought for impactful uses of patient data, collected with smartphones, in Parkinson's monitoring and treatment NEW YORK, Feb. 6, 2013 /PRNewswire-USNewswire/ --The Michael J. Fox Foundation (MJFF) is launching a $10,000 research challenge to spur ideas for using patient data, collected using smartphones, in Parkinson's disease (PD) monitoring and treatment. "Our Foundation is committed to developing opportunities for patients to contribute data about the real experience of Parkinson's disease, which researchers can leverage in pursuit of a cure," said Maurizio Facheris, MD, MSc, associate director of research programs at MJFF. "Many symptoms of Parkinson's disease can be simply and objectively measured with smartphones. We have such a data set and we're challenging the research community to help us put it to use." Mobile phones are some of the most pervasive types of monitoring devices, with smartphones carrying basic sensors that can be used to measure and monitor many features of PD to give a window into a patient's life. Researchers, collaborating entrepreneurs and industry experts at Gecko Ventures and MIT have developed a basic collection application, and collected data from a group of Parkinson's patients and control subjects. Now MJFF is challenging research teams to develop the best way … Continue reading →

KALAMAZOO, Mich., Feb. 7, 2013 /PRNewswire/ -- Metabolic Solutions Development Company, LLC (MSDC) announced today that it has received an award from The Michael J. Fox Foundation for Parkinson's Research (MJFF) to conduct preclinical research on a first-in-class mTOT Modulator, MSDC-0160, as a potential treatment for levodopa induced dyskinesia (LID). The study will be undertaken in collaboration with Patrik Brundin, MD, PhD, of Van Andel Institute (VAI). The aim of the study, titled "Potential of Novel Insulin Sensitizers to Treat Dyskinesia," is to determine if MSDC-0160 can prevent or reverse LID in a preclinical model of Parkinson's disease (PD). Should the results show that MSDC-0160 can significantly modify LID in vivo, MSDC plans to begin a clinical trial to examine the effects of MSDC-0160 in PD patients with LID. Such a clinical trial could begin in 2014. MSDC-0160MSDC-0160 is a novel once-a-day oral insulin sensitizer and the first in a new class of therapeutic agents called mTOT Modulators. mTOT is newly identified protein complex in the inner mitochondrial membrane that appears to function as a molecular "sensor switch" that coordinates carbohydrate, lipid, and amino acid metabolism. MSDC-0160 selectively modulates proteins in the mTOT complex, effecting pyruvate utilization and resulting in … Continue reading →

Feb. 6, 2013 Columbia University Medical Center (CUMC) researchers have identified a protein trafficking defect within brain cells that may underlie common non-familial forms of Parkinson's disease. The defect is at a point of convergence for the action of at least three different genes that had been implicated in prior studies of Parkinson's disease. Whereas most molecular studies focus on mutations associated with rare familial forms of the disease, these findings relate directly to the common non-familial form of Parkinson's. The study was published today in the online edition of the journal Neuron. The defective pathway is called the "retromer" pathway, in part because it can guide the reutilization of key molecules by moving them back from the cell surface to internal stores. In this study, defects in the retromer pathway also appear to have profound effects on the cell's disposal machinery, which may explain why Parkinson's disease brain cells ultimately accumulate large protein aggregates. The trafficking defects associated with Parkinson's can be reversed by increasing retromer pathway activity, suggesting a possible therapeutic strategy. No current therapies for Parkinson's alter the progression of the disease. The researchers also found evidence that, even in unaffected individuals who simply carry common genetic … Continue reading →

Findings implicate two genetic variants that disrupt protein sorting in neurons Columbia University Medical Center (CUMC) researchers have identified a protein trafficking defect within brain cells that may underlie common non-familial forms of Parkinsons disease. The defect is at a point of convergence for the action of at least three different genes that had been implicated in prior studies of Parkinsons disease. Whereas most molecular studies focus on mutations associated with rare familial forms of the disease, these findings relate directly to the common non-familial form of Parkinsons. The study was published recently in the online edition of the journalNeuron. The defective pathway is called the retromer pathway, in part because it can guide the reutilization of key molecules by moving them back from the cell surface to internal stores. In this study, defects in the retromer pathway also appear to have profound effects on the cells disposal machinery, which may explain why Parkinsons disease brain cells ultimately accumulate large protein aggregates. The trafficking defects associated with Parkinsons can be reversed by increasing retromer pathway activity, suggesting a possible therapeutic strategy. No current therapies for Parkinsons alter the progression of the disease. The researchers also found evidence that, even in … Continue reading →

Featured Article Academic Journal Main Category: Parkinson's Disease Also Included In: Genetics;Biology / Biochemistry;Alzheimer's / Dementia Article Date: 07 Feb 2013 - 3:00 PST Current ratings for: Non-Familial Parkinson's Cause And Treatment Clue Found In Three Genes 5 (2 votes) The researchers, from Columbia University Medical Center (CUMC) in New York, write about their findings in the 6 February issue of Neuron. Most people with Parkinson's disease have the sporadic, non-familial form of the disease, with a small proportion having familial Parkinson's, or the form that can be attributed to known genetic factors. The defect is in a pathway known as the "retromer" pathway, because it guides the recycling of key proteins by moving them back from the surface of the cell to its internal stores. The researchers found that defects in this pathway may disrupt the ability of cells to dispose of unwanted proteins, which may explain why brain cells of people with Parkinson's accumulate clumps of protein. They suggest the defects can be reversed by increasing pathway activity, offering a possible route to treatment. There are currently no treatments that alter progression of Parkinson's. They also found evidence that the molecular changes behind the defects in the retromer … Continue reading →