Articles tagged with Axons
Researchers designed nerve networks with varying widths to mimic brain connections, creating logic gates and biological clocks. They discovered a threshold thickness for axon development, allowing for the growth of around 100 axons, essential for signal transmission.
Researchers found that claudin 11 prevents charged ion leakage through myelin layers, increasing resistance and affecting signal conduction. This defect may be linked to cognitive deficits and neurodegenerative diseases, particularly in neurons with thin myelin sheaths.
Scientists have discovered that a protein banished from mature axons allows them to transform into dendrites. This process could occur after nerve cell damage, raising possibilities for the reverse transformation.
Researchers discovered that a rare genetic disorder, tuberous sclerosis complex, may be linked to neurological disorders such as autism, epilepsy, and mental retardation. The study found that abnormal neuronal structure can lead to excess brain connections, which may contribute to these conditions.
A Salk Institute team identified p75 as an unexpected factor that helps keep retinal axons from going astray. The protein previously known for regulating cell survival leads a double life as an axon guidance protein.
Researchers at Loyola Medicine report a potential treatment for stroke patients that could restore functions and reverse damage. The technique involves anti-nogo-A immunotherapy, which has improved lab animal results and is being tested in human clinical trials.
Researchers have developed a simple model to study injured brain tissue, enabling the induction of regeneration of axons. The fruit fly model has shown that activation of the JNK signaling pathway promotes nerve bundle repair.
Researchers developed a new MRI technique that can detect diffuse axonal injury, a type of brain damage often overlooked. The test analyzed water motion in areas surrounding nerve cells and found significant links to recovery rates.
During embryonic development, ephrin/Eph signaling helps regulate the growth of sensory and motor neurons. When this cross-talk is interrupted, motor neurons can mistakenly join sensory pathways, leading to a 'wiring disaster.' Researchers hope to use these findings to develop new treatments for spinal cord injuries
Neuroscientists discover that insulin-like growth factor (IGF) plays a critical role in setting up connections between chemical detectors in the nose and the brain's olfactory centers. IGF joins other molecules known to direct nerve cell growth, making it another tool for wiring up the brain.
Researchers found that axonal CREB plays a key role in transmitting signals from the growth cone to the nucleus, ensuring neuron survival. This discovery sheds new light on neural development and may have implications for treating neurological diseases such as Alzheimer's.
Researchers at MIT have identified a family of proteins essential for the formation of communication networks in the brain. The discovery could lead to therapies involving stimulation of neurite growth, repairing spinal column injuries or treating brain injuries or neurodegenerative disorders.
A study by Johns Hopkins Medicine reveals a subset of adult brain cells that can exhibit dynamic behavior, including elongation and morphing, unlike traditional adult axons. This discovery opens up new avenues for understanding neural recovery following stroke or other brain trauma.
Haesun Kim's research focuses on Schwann cells and axon communication links in myelination, which may lead to remyelination and correction of neurological disorders. The study aims to pinpoint the sequence and nuances of communication links involved in myelination.
Researchers found that axon stimulation can increase signal transmission to the cortex, suggesting a new mechanism for brain processing. This discovery may lead to treatments for psychiatric disorders where brain cells communicate incorrectly.
Researchers found a pair of proteins that facilitate communication between axons and glial cells, initiating myelination. Understanding this process may lead to new treatments for neurodegenerative diseases like MS.
A study published in PLOS Computational Biology reveals that noise effects in ion channels are much larger than previously assumed, compromising the fidelity of neural transmission. The researchers used detailed models and simulations to demonstrate how channel noise destroys information in action potentials.
A novel video-imaging system reveals that slow component-b proteins, involved in Parkinson's and Alzheimer's diseases, exhibit rapid bursts of movement followed by pauses. Multiple slow proteins are also transported together as 'packets,' piggy-backing on molecular motors, suggesting a potential carpooling mechanism.
A study found vulnerabilities in premature infants' brains similar to those in mature brains, but also identified a significant difference that suggests different treatments are needed. Damage occurs mainly in white matter, which connects brain regions, and can lead to behavioral problems and developmental delay.
The brain's information processing is more chaotic than previously thought, with neurons releasing chemical messengers along their entire length. This challenges traditional understanding of neuronal communication and may lead to new medical drug development.
A University of Utah study found that a mutant gene that affects nerve-cell elasticity may have contributed to spinocerebellar ataxia type 5 (SCA5), a disease previously linked to President Abraham Lincoln's family. The discovery raises the possibility that Lincoln himself may have had SCA5.
Researchers have found that motor protein myosin X travels along the actin filament of a neuron's backbone, delivering the DCC receptor to its periphery where it interacts with netrin-1. This process enables axons to grow in the right direction and form synapses.
Researchers at the University of Pennsylvania School of Medicine propose a new approach for brain-machine interfaces using undamaged nervous tissue to provide command signals to drive prosthetics. The system may one day enable people with spinal-cord injuries or limb loss to regain control over their devices.
Vanderbilt researchers have successfully produced movies that provide the first direct view of the initial stage of myelin sheath formation in nerves. The process is more dynamic than previously thought, with cells continually sending out tiny tentacles to readjust their positions.
In a surprise discovery, researchers found that young rats recover more quickly from spinal cord injuries due to the activation of specialized neural stem cells and oligodendrocytes, which provide a protective myelin sheath to axons. This process does not occur as efficiently in adult rats, leading to longer recovery times.
A new study has shed light on the mechanisms controlling myelin formation, a process crucial for efficient nerve communication. Researchers found that Par-3 acts as a molecular scaffold to organize key proteins essential for myelination.
A key gene, Boc, has been identified as crucial for brain neural circuit formation and axon guidance in the nervous system. This discovery could lead to novel strategies for treating neurodegenerative diseases such as Alzheimer's and Parkinson's, and spinal cord injuries.
Researchers at Brown University have identified a peptide that can spur cargo transport in nerve cells, shedding light on the complex intracellular transport system inside nerve cells. The discovery could help scientists better understand nerve cell function and test possible therapies for neurodegenerative diseases such as Alzheimer's.
Researchers have identified how the body's own immune system contributes to nerve fiber damage in multiple sclerosis. B-cells damage axons by inhibiting energy production, leading to degeneration and death. This finding could aid therapy development for this chronic disease.
Researchers have identified the JNK, Wnt, and FGF signaling cascades as the most important actors in axon growth, showing that growth is independent of neuronal activity. This finding brings greater clarity to the axon's growth process and has implications for understanding nerve diseases such as Alzheimer's and multiple sclerosis.
Researchers found that nicotinamide can protect against nerve damage in the chronic progressive phase of MS, preventing disability. Nicotinamide increased levels of NAD, which reduced neurologic deficits and protected axons from further degradation.
Scientists at Harvard University have developed nanowire arrays that can detect, stimulate, and inhibit nerve signals along individual axons and dendrites of live mammalian neurons. This breakthrough technology has the potential to revolutionize our understanding of brain activity and signal propagation in neuronal networks.
Researchers at Case Western Reserve University developed a method to bypass spinal cord injuries by regenerating severed nerve fibers and reconnecting them with the spinal cord. The treatment, using an enzyme called chondroitinase, resulted in improved mobility in rats with impaired motor functions.
Researchers developed an effective treatment using embryonic stem cells to restore motor function in paralyzed rats. GDNF was found to be a focal attractive cue for transplanted axons, facilitating the establishment of neuromuscular junctions and resulting in noticeable recovery.
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 at Salk Institute and Stanford University found that axon degeneration after injury involves different mechanisms than normal developmental pruning. The Wlds protein has been shown to slow degeneration in cut axons, and its conservation across species suggests general mechanisms for preserving nerve function.
Researchers have discovered a protein complex that regulates axon growth and development in the nematode worm Caenorhabditis elegans. The complex, composed of UNC-69 and UNC-76 proteins, plays a crucial role in maintaining normal presynaptic organization and regulating vesicle trafficking.
Researchers created a simple biophysical model of an axon that reproduced catastrophic oxidative stress-induced collapse, characteristic of neurodegenerative diseases. The study also revealed the role of free radicals and antioxidants in axon degradation.
Researchers at the University of Pennsylvania School Medicine have created a three-dimensional neural network that can be transplanted to bridge spinal cord lesions. The construct, designed to mimic the longitudinal arrangement of the spinal cord, integrates with host tissue and maintains its geometry after transplantation.
A gradient of Wnt3 counterbalances EphrinB1-EphB signaling to establish a carefully controlled pattern of nerve connections required for conveying spatial information from the eye to the brain. This balance is necessary for topographic mapping, which allows positional information to be smoothly transferred to the brain.
Selective serotonin reuptake inhibitors (SSRIs) increase nerve impulse-carrying axon density in the frontal and parietal lobes, controlling emotions and motivation. This growth may explain why antidepressants take time to work, with effects seen within hours but clinically meaningful results taking weeks.
Researchers from Max Planck Institute discovered that a small number of molecular motors can pull cargo particles over long distances. By working together, the motors can overcome their individual limitations and achieve remarkable feats.
Researchers identify neuregulin gene as key factor in myelin production, enabling faster neural transmission. The discovery opens possibilities for repairing damaged spinal cords and brain tracts.
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.
A study published in Neuron reveals that inhibitory cues affect nerve fiber growth by activating proteins that repel or steer the axon. The findings identify possible targets within axons to block inhibitory signals, enabling damaged axons to regenerate and potentially restoring nerve function.
Molecular messengers Erk-1 and Erk-2 bind to vimentin, protecting their phosphorus message from loss. This linkage enables the safe transmission of the message along the axon, reaching the cell body for healing.
A new laser scalpel allows for precise cutting of nerves in worms, enabling researchers to study the basic mechanisms of nerve regeneration. The technique involves making mutations in genes believed to be involved in nerve regeneration and observing the effects on regeneration following laser severing of the nerves.
Researchers have developed a femtosecond laser nanosurgery technique to study genetic and molecular factors controlling nerve regeneration in C. elegans worms. The technique allowed for precise axon severing, enabling rapid recovery of function and new insights into neural regeneration.
A study by researchers at the University of Pittsburgh Medical Center found that exposure to methylisothiazolinone (MIT), a common ingredient in shampoos and personal care products, can restrict the growth of axons and dendrites of immature rat nerve cells. This may have potentially damaging consequences for human development.
Researchers at Medical College of Georgia have found that an enzyme called focal adhesion kinase plays a crucial role in guiding axons across the midline of the spinal cord during development. This discovery provides new insights into normal nervous system development and offers potential targets for treating spinal cord injuries.
UCSB researchers have discovered that changes in lipid composition of myelin lead to the unraveling of MS. The study shows how myelin basic protein acts as a patch to fill holes and maintain insulation from the sheath. This new knowledge may suggest methods for treating MS before it progresses.
Scientists at the University of Pennsylvania School Medicine have induced axon growth rates of up to ten centimeters per week, defying previous understanding. The stretched axons maintained a normal internal structure and appeared invigorated by extreme growth, suggesting new mechanisms for neuronal physiology.
Researchers successfully stimulated nerve cell regeneration after spinal cord injury using a combination of treatments. The study showed that axons can regrow into a cell graft placed in the lesion site, extending into the spinal cord and surrounding tissue.
Researchers at UNC have identified a molecular pathway that promotes nerve growth and regeneration in the spinal cord. The study reveals how NGF stimulation regulates key proteins to assemble axons from microtubules, providing new potential targets for repairing spinal cord injuries.
Researchers at Georgetown University Medical Center have discovered that axons are highly sensitive to tiny changes in molecular gradients. This finding has significant implications for understanding neural development and regeneration. The team plans to further investigate the role of molecular gradients in guiding axon growth.
A new measurement method and microenvironment evaluation technique have been developed to study spinal cord nerve regeneration. The findings extend earlier Mayo Clinic research, showing that a biodegradable scaffold can support axon growth under different experimental conditions.
Researchers developed a two-pronged approach to stimulate nerve cell growth and overcome inhibitory proteins, achieving triple the axon regeneration achieved with growth factors alone. The technique aims to restore vision and treat spinal cord injuries, strokes, and neurodegenerative diseases.
Researchers discovered a protective protein, Wlds, that safeguards dopamine-axon connections in Parkinson's disease. The study revealed that while the protein protects axons, it does not prevent cell body damage, highlighting differences in degeneration processes.
Researchers discovered that a special protein called importin beta is produced at the site of damage in axons, facilitating the entry of molecules into the nucleus. Blocking this process inhibits nerve regeneration, highlighting the need to identify proteins containing the "healing message"
Researchers have found that nerve degeneration in spastic paraplegia is associated with abnormal mitochondria and impairment of axonal transport, highlighting a potential target for therapeutic interventions. The study suggests that preserving mitochondrial function may help prevent axonal loss in this devastating condition.