View clinical trials related to ALS.
Filter by:This study aims to establish a biorepository and phenotyping database to investigate longitudinal changes in ALS subjects. Blood, including DNA and RNA, cerebrospinal fluid (CSF) and electrophysiologic measures will be collected every 6 months over 1 and a half years. The database and specimen repository will be made available to ALS researchers on a merit basis.
The purpose of this study is to look for abnormal genes and gene expression profiles that help determine why a person develops amyotrophic lateral sclerosis (ALS) and related motor neuron diseases (MND) and why their symptoms present and progress with a particular pattern.
This is a human clinical study involving the isolation of autologous bone marrow derived stem cells (BMSC) and transfer to the vascular system and inferior 1/3 of the nasal passages in order to determine if such a treatment will provide improvement in neurologic function for patients with certain neurologic conditions. http://mdstemcells.com/nest/
ALS is a devastative disorder characterized by motor neuron degeneration. Median survival is 3 years after onset, but may vary from a few months to more than 30 years. Various factors have been suspected to play a role in such a variation, but recently, it has been described that regulatory T-lymphocytes (T regs) may mediate ALS progression and survival. Vitamin D is an hormone know to regulated T reg function in vivo and in vitro. It have recently demonstrated that vitamin D (VD) levels correlated with ALS prognosis. The investigator want to go further in the study of the immune processes that could modulate prognosis in ALS. This could allow proposing VD as a potential treatment of ALS in a future trial. More largely, this could reinforce arguments in favor of an immune intervention to attenuate the severity of this devastating disorder.
The purpose of this study is to determine if AC-1204 is safe and tolerated in subjects with ALS. The reason why the investigator wants to use AC-1204 in patients with ALS is to determine if, by taking AC-1204, the body will make substances called ketone bodies. Further, if AC-1204 is well tolerated, the investigators want to change the amount the participant takes, to determine if the amount of ketone bodies in the blood increase in accordance with increases in the amount of AC-1204 the participant takes. The investigators want to do this study because when the investigators gave AC-1204 to mice with ALS, findings suggest the disease course is altered for the better and that the cause of this change is due to the presence of ketones in the blood. If AC-1204 can be proven to be safe and able to cause ketones to increase in the blood, the investigators will likely do subsequent studies to determine if the presence of ketone bodies will slow or stop the progression of the disease. However, this study is not designed to determine if AC-1204 will stop or slow the progression of ALS. It is designed to only determine if patients with ALS can tolerate AC-1204, if ketone bodies are produced and if the amount of ketone bodies produced increases with increasing dose.
The purpose of this study is to determine the safety and tolerability of RNS60 in patients with Amyotrophic lateral sclerosis (ALS). Investigators will also measure the impact of RNS60 on several markers of neuro-inflammation, measured by blood biomarkers and positron emission tomography (PET) imaging.
This study aims to assess the presence and the intensity of voluntary and cough reflex in patients with amyotrophic lateral sclerosis (ALS), comparing the results with the healthy control group. The assessment of the cough is fundamental to verify the mechanism of airways protection which is particularly compromised in ALS patients. Objective parameters of voluntary and reflex cough would be measured by the spirometer. The reflex of cough would be elicited by a solution of citric acid through an ultrasonic nebulizer.
This research study is being done to find out if tocilizumab, also known as Actemra™, can help with Amyotrophic Lateral Sclerosis (ALS). The investigators also want to find out if tocilizumab is safe to take without causing too many side effects. Currently ALS has no cure and 2 modestly effective treatment to slow the progression of the disease. Although not the initial cause of ALS, the immune system plays a role in the death of motor neurons. The immune cells that participate in this process are stimulated by a substance called interleukin-6 (IL-6) whose effect is blocked by tocilizumab and thus, may slow the death of motor neurons and slow the disease.
This is a parallel group, single institution, prospective clinical study. The purpose of this study is to assess whether the Jawbone Up 24, a consumer based accelerometer, can be a feasible tool to study physical activity in cancer patients and patients with Amyotrophic Lateral Sclerosis (ALS).
Amyotrophic lateral sclerosis (ALS) is due to neurodegeneration of upper and lower motor neurons, leading to muscle atrophy, paralysis and death. However, there is growing evidence that interneurons involved in the gain regulation of spinal motoneuron (lower motor neurons) and in sensorimotor integration may participate in the pathogenesis of ALS. While sensory afferents in the peripheral nerve are traditionally thought to be unaffected at the beginning of the disease, diffusion MRI has revealed degeneration and demyelination of the posterior columns in the spinal cord of patients recently diagnosed with ALS, and there are sporadic reports of sensory involvement. Early alteration of the sensorimotor integration could participate to the degeneration of motor neurons and interneurons. The goal of the project is to further investigate sensorimotor integration at spinal level in human patients recently diagnosed with ALS, and to study whether an interneuron pathology could participate in ALS pathogenesis. Our project has first an interest for the fundamental research aiming at increasing basic knowledge of pathophysiology of ALS, and specifically on the functional effects of the underlying neurodegenerative mechanisms. By testing the excitability of spinal interneurons in patients recently diagnosed, and by doing so for clinically uninvolved muscles, we will be able to evaluate whether an interneuron pathology could be involved in ALS. Our results will help to understand better the chain reactions in the neurodegenerative processes that dramatically evolve until the death of all motor neurons. Our project has also an interest for the development of therapeutic approaches for ALS. Indeed, our methods will help to determine specific electrophysiological biomarkers that will help to evaluate quantitatively spinal and corticospinal neural processes: their changes during the course of the disease (follow-up study), the effect of therapeutic agents and/or rehabilitation methods on their excitability, and their repercussions on motor neuron activity (evaluation of therapeutics). Lastly, our methods could be tested in other neuromuscular diseases to determine possible differences in spinal neural activity. Indeed, the motor dysfunction common to several neuromuscular diseases can make it difficult to make a definitive diagnosis. The development of specific biomarkers is crucial for an early diagnosis, and to evaluate the best treatment for the patients as rapidly as possible.