Articles tagged with Motor Neurons
Two types of spinal cord neurons were identified as enabling skilled forelimb movement: excitatory interneurons for accuracy and inhibitory interneurons for smooth movement. The discovery may lead to understanding normal human motor function and potentially treating movement disorders.
Researchers discovered specialized astrocyte functions support specific neurons, contributing to neurodegenerative disorders like ALS. The study also found potential links to developmental disorders such as autism and schizophrenia.
A team of scientists at UCL and King's College London has developed a technique to restore function to paralyzed muscles using light-activated neurons created from stem cells. The method involves transplanting these motor neurons into injured nerve branches, which can be controlled by adjusting blue light pulses.
A University of Wisconsin-Madison researcher has pinpointed an error in protein formation that could be the root of amyotrophic lateral sclerosis. Motor neurons that control foot muscles are affected due to a shortage of one of three proteins in neurofilaments, leading to tangles and nerve fiber malfunction.
Researchers at Harvard University have discovered a link between ALS mutations and motor neuron hyperactivity, suggesting a new therapeutic target. The approved medication for epilepsy may be effective in reducing this hyperexcitability, paving the way for clinical trials.
Researchers aim to deliver GDNF into muscle cells using a viral vector to protect motor neurons and slow disease progression in a rat model of ALS. The study, led by Cedars-Sinai Regenerative Medicine Institute, could pave the way for a clinical trial if successful.
A new study by Nationwide Children's Hospital researchers has identified a potential culprit in the death of motor neurons in Lou Gehrig's disease. Inhibiting nuclear factor-kappa B (NF-ƘB) in microglia slowed disease progression by 47 percent, suggesting a new target for ALS treatment.
Researchers have found that a plant pigment called quercetin could help prevent nerve damage associated with spinal muscular atrophy (SMA), a leading genetic cause of death in children. Quercetin was shown to significantly improve health of nerve and muscle cells in tests on zebrafish, flies, and mice.
Researchers found that a plant pigment called quercetin could help prevent nerve damage associated with SMA. Quercetin treatment improved the health of nerve and muscle cells in zebrafish, flies, and mice.
A team of researchers at the University of Pennsylvania has made a groundbreaking discovery about how climbing fibers provide feedback to Purkinje cells, allowing them to detect legitimate error signals amidst random firing. This knowledge will be fundamental to future studies of fine motor control and learning.
A new study suggests that a high-calorie diet rich in carbohydrates and fat may help slow the progression of motor neuron disease (ALS). Patients who were mildly obese lived longer than those who lost weight as ALS progressed. The diets improved survival rates, with fewer adverse events and deaths from respiratory failure.
Researchers at Columbia University Irving Medical Center found a toxin released by star-shaped brain cells called astrocytes that kills nearby motor neurons, leading to neuron loss in human ALS models. The study suggests new potential for slowing down or stopping the destruction of motor neurons and improving drug targets.
Researchers at St. Jude Children's Research Hospital found that ALS-causing mutations disrupt RNA transport in nerve cells, leading to protein misassembly and cell death. The study provides a new focus for treating ALS, a neurodegenerative disease associated with muscle weakness and paralysis.
A study by Columbia University Medical Center researchers identified matrix metalloproteinase-9 (MMP-9) as a key factor contributing to motor neuron degeneration in amyotrophic lateral sclerosis (ALS). The findings suggest that MMP-9 inhibitors may offer a new therapeutic option for treating this incurable neurodegenerative disease.
Scientists at UCL Institute of Neurology identified a genetic mutation that leads to the production of toxic RNA molecules, potentially responsible for frontotemporal dementia and motor neuron disease. The build-up of these molecules may be key to causing the diseases.
Scientists found that BMAA inserts itself into neuroproteins by seizing transfer RNA, causing misfolding and aggregation. Adding extra L-Serine can prevent this process, offering a potential prevention method for ALS.
A new therapy has shown promising results in slowing the onset and progression of Lou Gehrig's disease, increasing survival rates by up to 39% in animal models. The treatment targets the SOD1 gene, which is mutated in some cases of familial ALS, and was administered via non-invasive delivery.
Researchers found that tactile and motor neurons respond to visual cues, allowing for dynamic processing of the brain's internal spatial image. This discovery has implications for paralyzed individuals using neuroprosthetic limbs, suggesting a more integrated brain-body experience.
A zebrafish model reveals defects in motor neuron transport leading to CMT's progressive weakness and long-term pain. Researchers seek funding to identify new treatments for the condition.
Researchers at Stanford University School of Medicine have identified mutations in genes that encode chromatin regulators, which may contribute to the development of sporadic ALS. The study found 25 de novo mutations, including five in chromatin regulatory proteins, which could serve as potential therapeutic targets.
A recent fish study has identified a key hormone that enables zebrafish to replace damaged motor neurons, which could aid research into neurodegenerative diseases like ALS. This discovery also sheds light on the development of motor neurons in human embryonic stem cells.
Researchers at Northwestern University have isolated and labeled motor neurons in the brain that die in ALS, allowing for the study of disease progression. The discovery paves the way for identifying potential treatments for the devastating neurodegenerative disease.
Researchers discovered a novel compound that promotes motor neuron survival, offering a new approach to treating ALS. The study used stem-cell-derived motor neurons and screened over 5,000 compounds, finding kenpaullone to be more effective than existing treatments.
A new stem-cell based drug screening technology has identified a compound that prolongs the life of motor neurons in both normal and ALS-affected cells. The study found kenpaullone, which inhibits HGK, an enzyme associated with motor neuron death, to be more effective than two failed drugs in human clinical trials.
Researchers from Ruhr-University Bochum have discovered that vitamin P can protect motor neurons from dying off in culture. Unlike BDNF, which has limited effectiveness and potential negative consequences, vitamin P triggers a different signaling pathway to promote survival of isolated motor neurons.
A study published in Nature Neuroscience reveals that oligodendrocytes play a significant role in the early stage of ALS, with changes occurring long before physical symptoms appear. Suppressing an ALS-causing gene in oligodendrocytes delays disease onset and prolongs survival.
Research reveals that VCP gene mutations disrupt energy production in cells, leading to mitochondrial dysfunction and increased vulnerability. This study sheds new light on the role of VCP in multiple neurological disorders.
Researchers created motor neurons and astrocytes from a patient's skin cells, revealing that abnormal TDP-43 protein causes astrocyte death. This finding provides fresh insight into the mechanisms of motor neurone disease, a devastating condition with no cure or effective treatment.
Researchers at Duke University Medical Center have identified a new brain circuit controlling whisker movements in newborn mice. The circuit reveals how motor neurons integrate inputs from the LPGi region of the brainstem to enable voluntary whisking behaviors, shedding light on neural control of finger movements in humans.
Scientists have successfully reprogrammed one type of neuron into another within the brain, challenging the long-held notion that neurons are immutable. This breakthrough has significant implications for treating neurodegenerative diseases such as ALS.
Researchers compared pharyngeal nervous systems of nematode Caenorhabditis elegans and predator/omnivore Pristionchus pacificus, finding large differences in neuronal connections. These differences reflect the fundamental differences in feeding behaviors between the two species.
A new study by LSUHSC researchers has found that the ability of a protein called FUS to bind to RNA is essential to the development of Amyotrophic Lateral Sclerosis (ALS). By mutating FUS and blocking its RNA binding, the team was able to suppress ALS-related neurodegeneration in fruit fly models.
Researchers at Johns Hopkins Medicine have identified a protein crucial for neuron organization in the developing retina, shedding light on how the eye detects light. Additionally, scientists found that a genetic defect can cause a 'traffic jam' in cellular materials within motor neurons, leading to progressive paralysis and death.
Researchers at NYU Langone Medical Center have identified two genes, Hoxa5 and Hoxc5, that establish the neuronal circuits required for breathing. The discovery could advance treatments for spinal cord injuries and neurodegenerative diseases like ALS.
A single type of neuron in Caenorhabditis elegans nerve cord encodes an entire sensorimotor loop, with feedback driving motion itself. The discovery reveals a sophisticated system allowing the worm to organize its movements through proprioceptive feedback.
Researchers discovered a new mechanism by which STAT3 helps prevent axon degeneration, a hallmark of neurodegenerative diseases. CNTF treatment stimulated STAT3 to inhibit stathmin, leading to increased axon growth and reduced breakdown in ALS patients.
Researchers discover that spinal muscular atrophy results from motor circuit dysfunction, not motor neuron or muscle cell dysfunction. The study identifies a novel molecular pathway and proposes potential therapies involving potassium channel blockers.
A recent study reveals a common RNA pathway that contributes to the degeneration of motor neurons in both ALS and dementia. The discovery provides a potential target for developing new treatments and offers insights into the normal function of key proteins involved in these diseases.
Researchers at UMass Chan Medical School have discovered a gene that influences survival time in amyotrophic lateral sclerosis (ALS). The study found that blocking the activity of EphA4 receptor substantially extends the lifespan of people with the disease. Additionally, a new ALS gene (profilin-1) identified last month works in conjun...
Researchers at Kyoto University's Center for iPS Cell Research and Application have successfully recreated ALS-associated abnormalities in motor neurons derived from patients' induced pluripotent stem cells. Anacardic acid was found to rescue certain ALS phenotypes in vitro, offering a promising lead for developing new drug treatments.
Researchers identified gene mutations in profilin that affect nerve cell structure and growth, shedding light on how ALS destroys cells. The study provides a new piece of the puzzle in understanding ALS mechanisms, supporting existing studies on cell cytoskeleton disruptions.
Researchers at UMass Medical School have identified a new genetic mutation that causes familial amyotrophic lateral sclerosis (ALS), a fatal neurological disorder. The discovery points to defects in a neuron's cytoskeleton structure as a potential common feature among diverse ALS genes.
Research finds that both brain and muscle cells require the protein LRP4 to ensure robust communication. Without it, communication is inefficient and short-lived, contributing to disabling disorders like myasthenia gravis. The study suggests that delivering LRP4 through gene therapy may help bolster insufficient levels in patients.
Researchers employ pluripotent stem cells to model spinal muscular atrophy, revealing cell death mechanisms and identifying potential pharmaceutical treatments. The study provides an important clue for developing medicines to reverse or prevent motor neuron cell death in patients with the disease.
Researchers propose a new theory that motor cortex neurons generate rhythmic signals to control arm movements, contradicting the long-held assumption of encoding external spatial information. This discovery has broad implications for neuroscience and may explain some of the perplexing aspects of brain activity in motor cortex.
Scientists at Washington University, Stanford University, and Columbia University identified rhythmic brain cell firing patterns coordinated across populations of neurons in the motor cortex. These patterns were linked to different kinds of shoulder muscle movements, providing new insights into the brain's control of movement.
Researchers at the University of Bristol identified a simple yet crucial neural pathway in Xenopus frog tadpoles that initiates swimming. This discovery sheds light on how locomotion starts and may lead to new treatments for movement disorders like Parkinson's disease.
Researchers have identified a genetic mutation in the DYNC1H1 gene as the cause of rare form of spinal muscular atrophy with lower extremity predominance. This disease affects nerve cells controlling muscles of the legs and has a good prognosis, although patients are moderately disabled.
Researchers create functional motor circuits outside the body using stem cell-derived neurons and muscle cells, enabling accurate measurement of synaptic activity. The study provides a proof-of-principle for understanding neurological disorders that impair motor functions.
Researchers found that low levels of plastin 3 are linked to movement problems in spinal muscular atrophy, a fatal genetic disorder. Adding plastin 3 back to motor neurons in zebrafish restored some swimming abilities and suggests that the protein's decrease contributes to the disease's characteristics.
Researchers discovered that Fasudil increases the size of muscle fibers and their connection to motor neurons, improving the movement of SMA mice. This treatment bypasses the genetic cause of spinal muscular atrophy (SMA) by targeting the ROCK intracellular signaling pathway.
A protein called biglycan is essential for stabilizing synapses at the neuromuscular junction, a process crucial for muscle control and long-term health. Research suggests that biglycan could be a potential therapy for motor neuron diseases such as spinal muscular atrophy and ALS.
Researchers found that repeated injections of human umbilical cord blood cells improved motor neuron survival, delayed disease progression, and increased lifespan in mice modeling ALS. The study suggests that low-dose cell administration could be beneficial for patients with ALS even after symptom onset.
Researchers halt progressive neuron degeneration in rat model of familial ALS by switching off mutant TDP-43 expression. Recovery is possible if intervention occurs before significant motor neuron degeneration.
Researchers have pinpointed a new genetic segment on chromosome 9 as the cause of familial motor neuron disease, with affected patients carrying hundreds of DNA repeats that disrupt multiple mechanisms in motor nerve cells. This discovery may lead to new blood tests for early detection and treatment avenues.
Researchers aim to clarify the role of alpha-synuclein in spinal muscular atrophy (SMA), a genetic disease causing muscle weakness and degeneration. A better understanding of SNCA's role may lead to new therapies for SMA, potentially identifying useful disease markers and advancing neuromuscular disease research.
Researchers at Columbia University Medical Center have discovered that two genes, FUS/TLS and TDP-43, work together to support motor neuron survival in familial ALS. The findings, published in the Journal of Clinical Investigation, suggest that therapies targeting these genes may offer new hope for treating familial ALS.
Scientists have identified a mutation in the SIGMAR1 gene associated with juvenile amyotrophic lateral sclerosis (ALS), affecting Sigma-1 receptors involved in motor neuron function and disease development. The study suggests that further exploration of this receptor may uncover potential therapeutic targets for ALS.
Researchers have created a new model of ALS using human cells from autopsied tissue, finding that astrocytes secrete toxic factors that cause nerve cell degeneration. The study suggests that inflammatory responses and SOD1 function contribute to both sporadic and familial ALS.
Scientists at Nationwide Children's Hospital have developed a human-cell-derived model of ALS that accurately mimics the majority of cases. The new model reveals that astrocytes may be releasing toxins that contribute to motor neuron degeneration, highlighting the importance of replacing these cells as a potential therapy target.