The discovery of agile molecular motors could lead to better ways to treat motor neuron diseases, which destroy motor neurons and control voluntary muscles. The proteins, dynein and dynactin, are able to move back and forth along a microtubule, providing the necessary maneuvering ability for effective long distance transport.
Researchers created a 'cookbook recipe' to restore lost nerve function using mouse embryonic stem cells, growth factors, and specific agents. The approach showed promising results in recovering paralysis in treated rats, with some regaining muscle strength and mobility.
Scientists successfully transplanted motor neurons into paralyzed rats, restoring function and improving hind limb grip strength. The study demonstrates the potential for treating spinal cord injuries and diseases like ALS.
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Researchers at Salk Institute identify growth factor FGF as molecule guiding axons to muscles, uncovering general principles of neuronal connections. This discovery may help restore movement in people with motor neuron diseases and improve understanding of autism spectrum disorders.
Researchers found that a high-caloric ketogenic diet slowed ALS progression in mice by promoting mitochondrial energy production and membrane stabilization. The study suggests that dietary interventions may offer new therapeutic options for ALS patients.
Researchers at the Salk Institute identified V1 neurons as crucial for controlling rhythmic movements in the spinal cord, which enables walking. Disabling these neurons slows down the movement, highlighting their importance in locomotion.
Researchers mapped Hox protein expression patterns to understand motor neuron wiring and diversification. The code governs columnar, divisional, and pool identities, enabling precise connections between neurons and muscles.
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A Northwestern University study using live-cell time-lapse spectroscopy clearly links the presence of mutant SOD1 protein aggregates with neuronal cell death in ALS. The research provides a new understanding of aggregate structure and composition, offering hope for developing genetic suppressors and therapeutics.
A team of scientists studied the motor network of marine snails and found that higher-order neurons employ a combinatorial mechanism to produce variations in movement parameters. This hierarchical architecture allows for the generation of large numbers of behavioral variants, a hallmark of brain function.
The study reveals that Rnf6 targets LIMK1 for degradation, controlling actin dynamics and axonal growth. Changes in Rnf6 levels can be restored by compensatory changes in LIMK1 expression.
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A team of researchers at the University of Chicago has identified a gradient of biochemical signals, including Wnt proteins and Ryk receptor, that guide nerve growth down the spinal cord. This discovery offers new insights into how to repair or replace damaged nerves in adults.
Researchers at the Salk Institute found that opposing chemical signals from neurotransmitters sculpt the developing nervous system by preserving synapses between motor neurons and muscle cells. This process helps eliminate unnecessary sites, allowing for more efficient neural connections.
Researchers used RNA interference to silence mutated SOD1 genes in ALS mice, reducing disease progression and improving neuromuscular function. This breakthrough suggests gene silencing as a potential therapy for incurable progressive neurological diseases like ALS and Parkinson's.
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Researchers have successfully grown functional motor neurons from human embryonic stem cells in a lab, providing a critical breakthrough for treating diseases like ALS. The discovery challenges the long-held assumption that stem cell differentiation occurs in linear fashion.
Researchers at the University of Georgia are developing a stem cell-based drug assay to identify promising treatments for Spinal Muscular Atrophy (SMA), a group of inherited diseases that destroy nerves necessary for voluntary muscle movement. The goal is to accelerate development of safe and effective treatments by late 2007.
A new study suggests that indoprofen, a previously banned pain reliever, can increase SMN protein production in human fibroblasts by 13 percent. This increase could potentially lessen the severity of symptoms for children with Spinal Muscular Atrophy (SMA), a leading genetic cause of infant and toddler death.
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Researchers have discovered new approaches to treating ALS using genetic techniques and growth factors. A study found that implanting cells to support motor neurons can help stave off the disease, while another team used RNA interference to silence a toxic mutant gene. VEGF was also shown to rescue motor neurons attacked by ALS.
A study by McGill scientists identifies a new function for the Runx1 gene in the development of hindbrain visceral motor nerve cells. These cells regulate internal environment stability and vital functions such as blood pressure and heart rate.
Researchers found that the mutant SOD1 protein selectively migrates to spinal cord mitochondria, triggering apoptosis and cell death. This mechanism provides potential insight into how ALS-linked mutations cause degeneration in affected tissues.
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Researchers at Johns Hopkins Medicine have successfully coaxed new motor neurons out of embryonic stem cells and into the spinal cords of paralyzed rats. The study, funded by various organizations, aims to overcome a major hurdle in clinical therapy for motor neuron diseases like ALS and SMA.
Researchers have detected a Senataxin gene mutation that may contribute to the degeneration of motor neuron cells in a rare form of ALS. This discovery opens up avenues of investigation for understanding and treating other forms of motor neuron diseases.
A new mouse model of SBMA has been created, showing that the abnormal androgen receptor interferes with vascular endothelial growth factor (VEGF) production, leading to motor neuron degeneration. The study suggests VEGF may play a pivotal role in protecting motor neurons from damage.
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Researchers discovered that neighboring non-neuronal cells can protect or rescue motor neurons from degeneration when they carry an ALS mutation. This finding suggests the potential of stem cell replacement therapy targeting non-neuronal cells to treat ALS. The study used mouse models with a mutation in the gene superoxide dismutase (S...
Researchers discovered that healthy astrocytes and glia can rescue motor neurons containing ALS-causing mutations from degeneration. The study suggests inserting healthy astrocytes into ALS patients may reduce or prevent motor-neuron degeneration.
Researchers at Project A.L.S. have successfully tested a gene therapy approach that delays disease progression and prolongs survival in a mouse model of ALS. The treatment uses an adeno-associated viral vector to express the IGF1 protein, promoting neuronal survival.
Researchers at the Salk Institute have developed a detailed model of how stem cells produce motor neurons, which could lead to new treatments for spinal cord injuries and diseases affecting motor nerve cells. The study demonstrates an unusually efficient yield of 60 percent motor nerves using two key gene and protein-regulated pathways.
Researchers have discovered a genetic link between specific mutations in the Dnchc1 gene and selective death of motor neurons, causing diseases like ALS. The study provides new insight into the pathogenetic mechanism underlying MND.
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A recent study found that individuals who were always slim or participated in varsity athletics had a higher risk of developing ALS and other motor neuron diseases. The researchers suggest that vigorous physical activity may contribute to the development of these conditions, but further studies are needed to confirm this association.
Researchers found elevated levels of ceramides and cholesterol esters in spinal cords of people with ALS, leading to motor neuron degeneration. Treating these lipids with a drug called ISP-1 may prevent this process.
Scientists have made a breakthrough in growing functioning motor neurons from embryonic stem cells, a crucial step towards regenerating nerve tissue lost to disease or trauma. The success of the experiments suggests that human motor neurons can be grown using the same approach.
Researchers have found a possible link between viral infections and a treatable form of ALS. Six patients with HIV developed symptoms of motor neuron disease after anti-HIV treatment, suggesting that the AIDS virus can cause a variant of classic ALS.
Researchers found upper airway sensory impairment in snorers and OSA patients, increasing the risk of obstructive breathing episodes. The study also showed partial reversibility of sensory changes with continuous positive airway pressure treatment.
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Researchers found a set of neurons in the supplementary eye field that react when an individual realizes they made a mistake, shedding light on self-control and cognitive processes. This discovery has implications for understanding schizophrenia, obsessive-compulsive disorder, and psychopathic behavior.
Researchers discovered that injured spinal neurons establish gap junctions to communicate with each other, but not with healthy neighboring cells. This finding suggests a new approach to re-establishing connectivity between neurons and muscle after peripheral nerve damage or spinal cord injury.
Researchers found that chronic alcohol abuse in late adulthood damages Purkinje neurons by reducing message traffic between neurons, but the damage is mostly reversible. The study also suggests a connection between alcohol-induced brain changes and abnormal movements seen in alcoholics, such as unsteady gait and tremors.
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A study funded by NIAAA found a common linkage between prenatal alcohol exposure and attention-deficit/hyperactivity disorder (ADHD), suggesting reduced dopamine neurons may contribute to hyperactivity. The research suggests both immediate and long-lasting effects on the brain's ability to focus.
Researchers at Northwestern University have halted motor neuron destruction and slowed ALS progression using GDNF gene therapy in laboratory mice. The approach may one day prove effective in treating humans with ALS.
A new study finds that certain brain cells can be stimulated to regenerate following a stroke, potentially treating memory disorders in stroke patients. Researchers discovered a 12-fold increase in the birth of new cells in rodents after stroke, which may lead to rewireing the brain and helping survivors recover lost memory function.
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A UK study found that decreasing food intake can help ward off age-related brain disorders such as Alzheimer's disease and Parkinson's disease. The research team led by Mark Mattson discovered that eating less made nerve cells in the brain more resistant to deterioration and death.
A team of researchers has identified the normal function of a protein associated with spinal muscular atrophy (SMA), an inherited neuromuscular disease that is the most common genetic cause of infant mortality. The study, published in the journal Cell, also developed cell-based assays to search for potential therapeutic compounds.
Researchers have found that cells in the developing limb provide a key signaling molecule that defines motor neuron identity. The study reveals that motor and sensory neurons express the same genes, suggesting a coordinating role for the target region in constructing proper connections within the spinal cord.
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Physicians at UPMC are evaluating LBS-Neurons for treating stroke patients with a clinical human neuron transplant. The transplanted neurons aim to improve damaged host neurons or replace destroyed ones, showing promise in correcting cognitive and motor deficits.
A Yale study reveals that information related to faces is processed in a specific region of the prefrontal cortex. The research found that neurons responding to faces were clustered in one area, called the inferior prefrontal cortex, and were able to maintain activity even after stimuli disappeared.
A mutated gene in the glutamate receptor family causes faulty nerve cells to die due to false detection of neurotransmitters. The discovery may help understand how to slow down or stop this process, preserving neurons.
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A study comparing cephalopod and gastropod nervous systems reveals that cephalopods have more rapid-acting electrical firing systems, enabling their high-speed swimming behavior. The key element of the findings involves sodium channels in motor neurons used for jet-propelled swimming.
A team of researchers has made a promising discovery using gene therapy to protect dopamine-producing neurons in the brain from Parkinson's disease. The study found that injecting a modified virus carrying a specific gene into the brain led to improved neuron survival rates.
Researchers found that nitric oxide synthase is activated within minutes after nerve cell damage in medicinal leeches, leading to regeneration. The study suggests NOS may aid in minimizing tissue damage and infection by flagging down microglia at the site of injury.
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A Johns Hopkins study found that motor nerve grafts were more effective in regrowing nerve fibers than sensory nerve grafts. This breakthrough may lead to improved treatments for individuals with facial nerve injuries and other nerve damage, allowing for the restoration of movement while minimizing numbness or paralysis.
Scientists discover mutant mice lacking a gene fail to form distinct layers in the cerebral cortex, leading to fatal seizures and neurological disorders. The study provides new insights into neuronal migration and signaling pathways, potentially leading to breakthroughs in understanding human brain conditions.