Articles tagged with Motor Neurons
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Researchers discovered that an inorganic polyphosphate released by nerve cells contributes to the death of motor neurons in people with ALS and frontotemporal dementia. The study found that lowering levels of this toxin may be an innovative therapeutic strategy for diverse types of ALS/FTD.
The Precision ALS programme aims to provide new insights into Motor Neuron Disease through advanced data-driven prediction models and next-generation data analysis. The project will harness AI to analyse large amounts of data from a multimodal dataset, providing tools for clinical trials based on precision-medicine.
Researchers discover a genetic mechanism linking ALS and dementia to UNC13A protein corruption, providing hope for new treatments by blocking corrupted instructions. The study found that genetic variants increase the risk of UNC13A mRNA corruption in patients with ALS and FTD.
A new study from the University of Copenhagen has made significant breakthroughs in treating Parkinson's disease by targeting specific neurons in the brainstem. By stimulating excitatory neurons in the caudal area of the pedunculopontine nucleus, researchers were able to restore normal walking function in mice with Parkinson's symptoms.
A study in mice reveals how the Kdm6b gene influences motor neuron development into subtypes with distinct synaptic targets. The research, led by biologists at the University at Buffalo, founds that Kdm6b works cooperatively with proteins Isl1-Lhx3 to diversify motor neurons.
Researchers at MIT found that different types of dendrites process incoming information in distinct ways before sending it to the neuron's body. This specialization enables neurons to integrate various inputs and generate an appropriate response, particularly in navigation and planning movements.
A new cloud-based data resource has been developed to help identify new subtypes of amyotrophic lateral sclerosis (ALS), a fatal neurological disorder. The tool, part of the Answer ALS collaborative effort, uses biological and clinical data from over 1,000 patients to better understand the disease.
Researchers at the University of Pittsburgh have discovered how 'polyglot' neurons encode and decode sensorimotor chatter, enabling the differentiation between motor and sensory signals. This breakthrough has vital applications in brain-computer interfaces and neuroprosthetics, where accurate decoding is crucial.
Dartmouth researchers identified a new type of neuron in the rat brain that facilitates visual and spatial processing by tracking visual landmarks. The postrhinal cortex neurons can fire in two directions depending on the environment, allowing rats to estimate their direction.
A new meta-analysis of available literature on ALS disease has identified a group of seven environmental chemicals as correlates with increased risk of developing ALS. Exposure to these chemicals, including BMAA and heavy metals, may be contributing to the disease burden in certain regions.
A phase 3 clinical trial is underway to test the safety and efficacy of jacifusen, an experimental drug that lowered levels of toxic protein FUS in a patient with juvenile ALS. The trial aims to determine if the drug can slow disease progression in symptomatic patients.
In a study published in Cell, researchers report that ventral spinocerebellar tract neurons (VSCTs) are both necessary and sufficient for regulating locomotor behavior in mice. Activation of VSCTs induces locomotion, while suppression halts it, demonstrating their crucial role in controlling this essential behavior.
Researchers have discovered four distinct patterns of brain network disruption that reflect the underlying disease process in motor neuron disease (MND). These patterns are predictive of how the disease progresses and can be identified using electroencephalography (EEG), which may lead to more effective treatments.
Researchers at OHSU have discovered a unique neural cell assembly that enables complex learning in songbirds, similar to those found in the human primary motor cortex. This finding has implications for understanding fine motor control and may lead to new avenues for treating disorders such as ALS.
Researchers found that people with ALS have higher levels of arachidonic acid, a lipid involved in inflammation, and that tampering with this pathway can reduce muscle-weakening symptoms. The study suggests that targeting the arachidonic acid pathway may offer potential new therapies for Lou Gehrig's disease.
A new study found that cardiopulmonary bypass can significantly impact the development of brain cells in neonates, potentially leading to long-term neurocognitive disabilities. The research used a pre-clinical model to investigate the effects of cardiopulmonary bypass on brain growth and development.
Researchers published safety and efficacy data for a novel nusinersen drug delivery method via subcutaneous intrathecal catheter system (SIC) for spinal muscular atrophy (SMA) patients. The study found improvements in arm and hand function, but no significant changes in motor scales or muscle force.
Researchers identify 116 types of cells in the primary motor cortex, a significant step towards creating a comprehensive brain atlas. The findings aim to understand how neural networks control movement and cognition, and could lead to new therapies for neurologic and neuropsychiatric diseases.
A study published in Cell Metabolism identified a protein called neurturin as crucial for muscle health, improving metabolic rates, motor function and exercise capacity. Mice genetically modified to produce more neurturin had increased resistance to degeneration in neurons associated with ALS.
A new study from Salk Institute researchers found that a critical threshold of miR-218 levels determines the development of ALS in animal models. The study sheds light on the complex control of gene expression and its implications for treating neurological disorders.
Researchers at The Francis Crick Institute successfully reversed a key hallmark of motor neurone disease by blocking the activity of an enzyme called VCP. This breakthrough, published in Brain Communications, suggests that the abnormal accumulation of proteins involved in RNA regulation might be a factor contributing to the disease.
Researchers at Boston Children's Hospital report positive results with risplidam, a small-molecule drug that treats SMA by correcting the root cause: a mutated gene. Infants receiving risplidam showed improvements in motor function and lived longer than expected.
A new study by Texas A&M University researchers determines the minimum size of electrical currents needed to provide sensation in different parts of the mouth. They developed an equivalent circuit of the intraoral cavity and plan to investigate how electrical stimulation affects chewing and swallowing behaviors.
Dr. Brian Clark, Ohio University professor, has received a five-year, nearly $3 million NIH grant to investigate age-related changes in motor neuron excitability. The study will examine the role of motor neurons in health and disease, with potential implications for developing interventions to improve physical function in older adults.
A mutation in the C9orf72 gene may disrupt communication between motor neurons and muscles in ALS patients, leading to motor disorders, muscle atrophy, and mortality. The study reveals that the loss of function induced by the mutation affects synaptic transmission and protein TDP-43's location within the cell.
Researchers at Cedars-Sinai are conducting a clinical trial to transplant neural progenitor cells into the brains of ALS patients to slow disease progression. The cells have been genetically reprogrammed to express GDNF, which may help keep motor neurons healthy and extend survival.
Researchers have identified a potential new treatment for ALS using motor neurons created from ALS patients. The high-throughput platform confirmed two known targets and found an existing class of drugs that could reduce hyperexcitability, a key feature of the disease.
A live-cell screening strategy identified Kv7.2/7.3 as a key target for treating hyperexcitability-induced neurodegeneration in ALS patients. QurAlis' therapeutic candidate QRL-101 (QRA-244) shows promise in decreasing spinal and cortical motor neuron excitability.
A new study found that networks of nerve cells in the spinal cord called inhibitory interneurons lose connection to motor neurons, which could explain why motor neurons die in ALS. This loss happens before motor neuron death and affects fast-twitch motor neurons first.
Researchers link C9ORF72 mutations to neuronal death in familial ALS patients by discovering a toxic mechanism that blocks cellular processes involving DNA and RNA. The newly identified mechanism reveals how arginine-rich proteins displace essential proteins, leading to cell death.
A recent NIH study has identified a diverse range of motor neurons along the spinal cord that govern movement, including subtypes susceptible to neurodegenerative diseases. The research provides an atlas of 21 neuron types, offering new understanding of how these neurons control movement and contribute to organ systems.
Researchers created mini-chambers on a microfluidic device where human motor neurons and skeletal muscle cells grew, forming neuromuscular junctions. The study found that ALS motor neurons formed fewer connections and regenerated axons less efficiently than healthy ones.
Researchers found that brain diseases like Alzheimer's and Parkinson's affect men and women differently. The study suggests that accounting for sex differences in research leads to better results.
Scientists at Northwestern University have identified a compound that eliminates degeneration of upper motor neurons in ALS, a neurodegenerative disease. After 60 days of treatment, diseased brain cells regain health and function like healthy control neurons.
Researchers discovered that D1 and D2 neurons work together to perform reaching-and-grasping tasks, with D1 providing the early movement phase and D2 providing the final approach. This study sheds light on the complex mechanisms underlying motor function in the basal ganglia.
Researchers used a non-invasive imaging technique to measure mitochondrial function in patients with MND, finding phosphocreatine levels depleted and inorganic phosphates elevated. This technique could help assess the effectiveness of treatments for MND.
A study published in Nature reveals that a specific region of the brainstem is responsible for various fine motor activities of the forelimbs. The researchers used optogenetic and viral methods to mark neurons and observe their activity, identifying four neuronal subpopulations correlated with specific functions.
Ezogabine, an antiepileptic drug, has been shown to reduce motor neuron excitability in people with amyotrophic lateral sclerosis (ALS), a progressive neurodegenerative disorder. The study's findings could lead to the development of new therapies for ALS and establish the use of neuron excitability metrics as valuable biomarkers.
Research reveals basal ganglia neurons primarily use firing rate changes to control voluntary movements, with synchronized activity having a minor role in healthy conditions. Parkinson's disease symptoms may be improved by targeting abnormally increased correlated activity in the basal ganglia.
A Northwestern University research team discovered a highly ordered relationship between inhibitory neurons and motor neuron activity in zebrafish, revealing a compartmental scheme to regulate different speeds of movement. This finding provides insight into human movement disorders such as Parkinson's disease and epilepsy.
Melbourne researchers have identified the primary immune pathway triggered by TDP-43 accumulation in MND patients, paving the way for a new treatment. By blocking the STING immune sensor, they can prevent inflammation and promote motor neuron survival, offering a vital first step towards a treatment therapy.
A new study identifies NEMF as a driver of motor neuron diseases, linking defective protein quality control to motor neuron death. The research suggests that dysfunction of ribosomal quality control causes neurodegeneration, providing strong evidence for the link between protein quality control and human disease.
Research using a mouse model of DiGeorge syndrome found misfiring motor neurons responsible for tongue movement, leading to swallowing difficulties. The study aims to improve function in young children with difficulty eating or making sounds.
MDC researchers are using neuromuscular organoids to investigate how ALS mutations cause motor neuron death. They will sequence the organoid tissue samples to understand RNA activity in space and time, aiming to identify potential interventions or treatment targets for the incurable disease.
Researchers at the University of Tokyo have shown that a treatment enhancing neuromuscular junction (NMJ) formation can improve motor function and muscle strength in aged mice. The study's findings suggest that this approach may be effective in treating age-related motor impairment and muscular weakness.
A new study suggests that early treatment can help prevent permanent nerve damage and improve recovery in children with less severe forms of spinal muscular atrophy (SMA). German researchers recommend early screening for SMA using newborn screening programs to identify children who may benefit from earlier treatment.
Scientists have discovered that a mutant protein associated with familial ALS disrupts neurotransmission at the squid giant synapse. Intermittent high-frequency stimulation restores synaptic function, suggesting a new approach to therapeutic intervention for ALS. This study provides insights into fundamental synaptic physiology and off...
A study found that replenishing the SV2 protein can restore synaptic function and prevent cells from dying in a genetic form of ALS. This suggests that SV2 is a promising therapeutic target for slowing disease progression and prolonging muscle strength.
Researchers investigated how stress granules assemble and dissolve, shedding light on their role in neurodegenerative diseases like ALS. Stress granules formed in response to stress can promote the assembly of dynamic structures that may trigger motor neuron death.
A team of researchers from the University of Toronto has delayed the onset of amyotrophic lateral sclerosis (ALS) in mice by preventing neuron degeneration. The result, combined with other clinical advances, holds promise for a potential treatment for ALS in humans.
A recent study published in Autonomic Neuroscience: Basic and Clinical reveals the extent of connections between the small intestine and the entire brain. Half of the neurons transmitting signals from the gut to the brain also send motor signals, enabling cross-talk within the same neuron.
Researchers discovered that TBK1 mutations in mice with ALS-like symptoms initially slow disease progression but later accelerate it. The study sheds light on the complex relationship between ALS genetics and its mechanisms, highlighting challenges in developing safe treatments.
Researchers at NCBS discovered that dopamine released by nerve cells activates faster motor neurons, allowing zebrafish to swim faster. This finding suggests motor neuron plasticity can be exploited for rehabilitation after spinal cord injury or stroke.
Researchers found that degrading perineuronal nets improves learning abilities in mice but disrupts memory storage. Children's brains have flexible connections allowing for better learning and recovery from brain injury due to intact perineuronal nets.
Researchers successfully reproduced key ALS symptoms in zebrafish using optogenetic TDP-43, a human protein that forms aggregates upon blue light exposure. The study reveals motor neurons may be damaged before TDP-43 aggregation, suggesting new avenues for ALS treatment.
Researchers at Karolinska Institutet have discovered a gene, Synaptotagmin 13, that protects against motor neuron degeneration in ALS and SMA. Gene therapy was shown to increase life expectancy in animal models.
Astrocytes, a type of cell that supports motor neurons, play an important protective role in the early-stages of sporadic motor neuron disease. When close to motor neurons, these cells help rescue them from misfolded protein TDP-43.
A new study identified Gemin3 as a molecular 'bridge' between genes causing amyotrophic lateral sclerosis (ALS), a neurodegenerative disease. The research holds promise for developing treatments effective for a broad range of ALS patients.
Researchers developed a novel gene-silencing approach to deliver a treatment vector to adult ALS mice, preventing disease onset and blocking progression in animals with existing symptoms. The method uses an adeno-associated virus to deliver shRNA, effectively silencing the SOD1 gene and protecting motor neurons.
A study published in the Journal of Neuromuscular Diseases found Nusinersen treatment improved motor and respiratory functions in adults with longstanding SMA3. Functional testing showed significant improvements on the 6-Minute-Walk-Test, with patients experiencing a mean improvement of 8.25 meters.