Plans to trial transplanting pig cells into the brains of New Zealanders with Parkinson's disease have cleared a major hurdle with the Ministry of Health granting ethical approval. The ministry's health and disability ethics committee granted approval ahead of trials due to begin in the first quarter of next year, the company behind the trials, Living Cell Technologies (LCT), said on Friday. Medsafe gave LCT regulatory authorisation last month. It took about two years for LCT to get ethical approval following regulatory authorisation in 2007 for its pig cell diabetes treatment trial. "We are extremely pleased to have received ethical approval in such an efficient timeframe," said LCT managing director Andrea Grant. LCT will now need to get a good manufacturing practices licence for the trial to proceed. Pre-clinical trials suggest the Parkinson's treatment, known as NTCELL, can protect brain tissue which would otherwise die, potentially delaying or preventing the effects of the neurodegenerative disease. Only those who have been diagnosed with Parkinson's for at least four years will be part of the study, which will last for up to 60 weeks. Read more: Ethical approval for pig cell brain trial … Continue reading →

Protein clumps called Lewy bodies (centre) found in Parkinsons disease are caused as misfolded -synuclein moves from cell to cell. Kelvin Luk/Univ. Pennsylvania/Science AAAS The catastrophic damage wreaked by a rogue protein involved in Parkinsons' disease has been tracked by researchers, in work that might help to reinvigorate an old treatment strategy to slow the condition. A team led by Virginia Lee, a neurobiologist at the University of Pennsylvania in Philadelphia, injected a misfolded synthetic version of the protein -synuclein into the brains of normal mice and saw the key characteristics of Parkinsons disease develop and progressively worsen. The study, published today in Science1, suggests that the disease is spread from one nerve cell to another by the malformed protein, rather than arising spontaneously in the cells. The finding raises the possibility that an antibody that binds the misfolded -synuclein could be used to intercept the protein as it passes between nerve cells. Its very hard to ask antibodies not only to get inside the brain, but to get inside cells, says Lee. But now you have the possibility of stopping the spreading. And if you stop the spreading, perhaps you can slow the progression of the disease. The idea … Continue reading →

JERUSALEM, Nov. 13, 2012 (GLOBE NEWSWIRE) -- Further to Brainsway's (BRIN.TA) announcement regarding the association between Brainsway and Advanced Technologies Innovation Distribution SRL ("ATID") for the marketing and sales promotion of Brainsway's Deep TMS devices in Italy, in the context of which ATID has been conducting - among its other activities - clinical trials in the San Raffaele medical center in Milan, Italy, the Company is pleased to announce the following clinical trial results: 1. Clinical trial to evaluate the safety and efficacy of a specialized Deep TMS therapy for Parkinson's disease patients. The trial was carried out in two phases. The first was a double-blind placebo-controlled phase. The data from this phase are still being analyzed. The following are the final results of the second, open-label phase of the trial, in which all patients received REAL Deep TMS treatment. The trial included 27 Parkinsonian patients who received 12 high-frequency Deep TMS treatment sessions over the course of 30 days. Analysis of patients' scores on the motor section of the Unified Parkinson's Disease Rating Scale (a commonly used scale for rating the severity of Parkinson's disease symptoms) revealed a significant improvement in severity of motor symptoms compared to the patients' … Continue reading →

We recruited patients from five centres in the Netherlands who were aged 18 years or older, had idiopathic Parkinson's disease, and had, despite optimum pharmacological treatment, at least one of the following symptoms: severe response fluctuations, dyskinesias, painful dystonias, or bradykinesia. By use of a computer-generated randomisation sequence, we randomly assigned patients to receive either GPi DBS or STN DBS (1:1), applying a minimisation procedure according to drug use (levodopa equivalent dose vs 1000 mg) and treatment centre. Patients and study assessors (but not those who assessed adverse events) were masked to treatment allocation. We had two primary outcomes: functional health as measured by the weighted Academic Medical Center Linear Disability Scale (ALDS; weighted by time spent in the off phase and on phase) and a composite score for cognitive, mood, and behavioural effects up to 1 year after surgery. Secondary outcomes were symptom scales, activities of daily living scales, a quality-of-life questionnaire, the occurrence of adverse events, and drug use. We used the intention-to-treat principle for all analyses. This trial is registered with http://www.controlled-trials.com, number ISRCTN85542074. Follow this link: Subthalamic nucleus versus globus pallidus bilateral deep brain stimulation for advanced Parkinson 's disease (NSTAPS ... … Continue reading →

ScienceDaily (Nov. 15, 2012) Understanding how any disease progresses is one of the first and most important steps towards finding treatments to stop it. This has been the case for such brain-degenerating conditions as Alzheimer's disease. Now, after several years of incremental study, researchers at the Perelman School of Medicine, University of Pennsylvania have been able to piece together important steps in how Parkinson's disease (PD) spreads from cell to cell and leads to nerve cell death. Their line of research also informs the general concept that this type of disease progression is a common pathway for such other neurodegenerative diseases as Alzheimer's, Huntington's, progressive supranuclear palsy, and possibly amyotrophic lateral sclerosis (ALS). The Penn team found that injecting synthetic, misfolded and fibrillar -Synuclein (-Syn) -- the PD disease protein -- into the brains of normal, "wild-type" mice recapitulates the cascade of cellular demise seen in human PD patients. Parkinson's disease is characterized by abundant -Syn clumps in neurons and the massive loss of midbrain dopamine-producing neurons. However, a cause-and-effect relationship between the formation of -Syn clumps and neurodegeneration has been unclear. In short, the Penn researchers found that, in healthy mice, a single injection of synthetic, misfolded -Syn fibrils … Continue reading →

Carol and Mike Werner/Photo Researchers Digital illustration comparing dopamine levels in a normal neuron and one affected by Parkinson's disease. The Parkinson's affected neuron on the left produces a very low level of the neurotransmitter dopamine. The neuron on the right supplies a normal amount of dopamine to the synapse. A rogue protein injected into the brains of mice led to a cascade of effects that culminated in Parkinsons-like symptoms in an experiment that may, for the first time, establish the diseases path of destruction. Healthy mice injected with the abnormal protein began producing it in their brains, leading to clumps of the substance called Lewy bodies. The clumps in turn caused loss of dopamine- producing neurons that are key to motor control, according to a study in the journal Science. Loss of the nerve cells causes difficulty in moving, a trait of Parkinsons disease. Both Lewy bodies and loss of dopamine-producing neurons had been linked to the illness. Until now, it wasnt clear how the two were linked together, said study author Virginia M.-Y Lee, the director of the Center for Neurodegenerative Disease Research at the University of Pennsylvania. You have a bad protein in a bad shape, and … Continue reading →