Articles tagged with Axons
Researchers at UofSC have identified a molecular pathway that promotes nerve regeneration in the central nervous system, bridging the recovery gap between peripheral and central nerves. The discovery could lead to new treatments for spinal cord and brain injuries.
Researchers at HKUST found a way to stimulate axon growth without external stimulants. The deletion of the PTEN gene enhances compensatory sprouting and promotes regeneration of CST axons. This breakthrough study offers new possibilities for treating chronic SCI, including delayed treatment up to 1 year after injury.
Researchers found that nerve cells act as barriers or guides to position themselves correctly, creating a map for other cells to follow. This study uncovers an exciting new mechanism for how nerve cells position themselves in the first place, with important implications for understanding neurodevelopmental disorders.
Researchers discovered a key protein, Sema6A, that helps guide axons from neurons in the retina to the correct part of the brain. This finding has implications for treating eye movement disorders and regenerating damaged vision-sensing nerve cells.
Researchers at UC San Diego School of Medicine found that axon injury location affects regeneration in neurons. Injury before a branch point resulted in 89% regeneration, while cuts to both branches led to 67% regeneration.
Scientists have developed a 'Neuronal Positioning System' that maps the axonal wiring of individual neurons, revealing organizational principles of neuronal networks. This new approach enables researchers to study how specific neurons are wired to other types and regions, providing insights into brain function and development.
A team of biologists at Vanderbilt University has identified a specific signaling protein called Asef2 as crucial for forming dendritic spines, the tiny filaments that connect neurons to enable memory formation. This discovery could lead to new treatments for autism and Alzheimer's diseases.
Scientists have discovered a protein called SARM1 that triggers axon degeneration after an injury, leading to a rapid decline in energy supply within axons. Supplementing neurons with a precursor to NAD, nicotinamide riboside, can block axon degeneration and neuron cell death.
Using mathematical models, researchers show that externalizing the cell body increases electrical signal transmission at no additional energetic cost. This design allows for efficient transmission of small input signals to neighboring cells.
Researchers discovered that increasing brain activity can stimulate myelin production, which protects nerve fibers. This finding could lead to new treatments for multiple sclerosis.
Researchers at IRCM have uncovered a new synergy mechanism required for neural circuits to form properly. This breakthrough may lead to the development of tools to repair nerve cells following injuries to the nervous system.
Researchers identified a gene called Gpr56 that regulates nerve cell insulation in the central nervous system. Without proper insulation, nerve cells can't transmit signals efficiently, leading to diseases like multiple sclerosis.
Two studies found a unique molecule that can repair damaged nerve cells by locating and clearing out bad cells. The phosphatidylserine receptor (PSR-1) also helps reconnect broken nerve fibers in the regeneration process.
A new drug called ISP was designed to mimic a critical part of an enzyme found in damaged axons, promoting recovery from spinal cord injuries. Injections of the drug partially restored axon growth and improved movements and bladder functions in paralyzed rats.
A team of researchers has identified a chemical compound called indazole chloride that can decrease the effects of multiple sclerosis. Ind-Cl works by inhibiting selective inflammation and remyelinating axons, restoring neuronal function and potentially reducing MS progression.
Researchers at UT Arlington's Biophysics and Physiology Lab developed new methods for optogenetic stimulation of brain neurons, guiding axons to form loops in the lab. The advancements aim to map neural circuitry and potentially treat conditions like chronic pain and drug addiction.
Researchers at the University of Bonn discovered a previously unknown nerve cell shape that allows signals to be transmitted directly from dendrites to axons, bypassing the cell body. This unique structure facilitates faster and more efficient communication between neurons.
Researchers found that an inside-out vein graft filled with platelet-rich plasma (PRP) improved sciatic nerve function in rats compared to traditional autografting. The study showed increased myelination, axon diameter, and myelin sheath formation in PRP-filled vein grafts.
Researchers have solved a longstanding puzzle in neuroscience by revealing the three-dimensional atomic structure of netrin-1, a guidance protein that can attract or repel brain cells. By understanding how this protein works, scientists may be able to develop new ways to steer cell behavior and potentially treat diseases such as cancer.
Researchers at University of California, San Diego School of Medicine and Veteran's Affairs San Diego Healthcare System report that neurons derived from human induced pluripotent stem cells (iPSC) extended tens of thousands of axons across the rats' central nervous system. The study suggests a promising approach for treating spinal cor...
Research by Prof. Peter W. Baas highlights the importance of microtubules in facilitating nerve regeneration following injury. The study demonstrates that microtubule-based strategies can promote axonal growth and regeneration, particularly in the distal tip of the axon.
Researchers propose combining axon regeneration with relay strategies to restore spinal cord injury function. Introducing a new host or graft-derived neuron is necessary to reestablish neuronal pathways and relay supraspinal signal transmission to target neurons.
The study reveals that early neurons make many connections but correct mistakes, while later neurons are highly accurate in their target selection skills. The findings provide insight into normal brain development and have implications for understanding autism and other disorders.
Researchers at the University of Western Australia discovered that soluble NRG1 plays a role in early peripheral nerve regeneration phases, promoting axon degeneration and regrowth. Soluble NRG1, already used in human trials for heart failure treatment, may be an effective therapeutic candidate to promote nerve regeneration.
Researchers found that combining a deacetyl chitin conduit with short-term electrical stimulation promotes better peripheral nerve repair. The treatment showed improved nerve conduction velocity, myelination, and axon diameter compared to non-stimulation group.
Researchers at Scripps Florida have shed light on the complex process of nerve cell growth, revealing a key protein's role in regulating axon extension. The study shows that RPM-1 coordinates the growth of axons with synaptic connection construction, providing new insights into neuronal development.
A new study published in TVST found that glaucoma is controlled by the brain, not the eye. The research shows that as previously disabled optic nerve axons recover, the remaining areas of permanent visual loss coincide with the areas that can still see in the other eye, forming a jigsaw puzzle-like pattern.
Developing neurons use the receptors DCC and neogenin to detect Netrin-1, guiding their growth towards anatomical boundaries. This understanding may lead to the development of drugs for spinal cord or brain injuries.
A new study by Harvard neuroscientists reveals that myelin, the electrical insulating material in nerve cells, is not uniformly distributed along axons. Instead, more evolved neurons in the cerebral cortex have intermittent myelin patterns, which may enable increased neuronal communication and complex behavior.
Brown University scientists found that the fundamental neural wiring map between the nose and brain becomes established in early development and remains unchanged throughout life. The study's findings provide insight into neurodevelopmental disorders and may have implications for regenerative medicine.
Basket cells convert excitatory signals into inhibitory outputs within milliseconds; researchers identify controlled increase in Na+ channels and conductance for fast transmission. Signal processing is made possible by high density of Na+ channels and increased conductance, compensating for small axon diameter and lack of myelination.
Critical illness polyneuropathy and myopathy involve sensorimotor axons and skeletal muscles, respectively, differing from Guillain-Barré syndrome in clinical manifestations. The study highlights the importance of differentiating critical illness polyneuropathy/myopathy from Guillain-Barré syndrome.
A team of researchers at the University of Pennsylvania has used mathematical modeling to better understand the mechanisms involved in traumatic brain injuries. Their findings reveal that rapid impacts can cause permanent damage due to the rate of stretching, not just the force applied.
Scientists have found a way to regrow dendrites, the branch-like structures of neurons that receive information from the brain, independently of axon regeneration. This discovery has significant implications for treating conditions like stroke, where damaged dendrites can only be repaired if blood loss is brief.
Researchers identified a key molecule facilitating transport of protein from neuron cell body to axon, enabling electrical impulses. This discovery could help explain neurological disorders linked to malfunctioning or degenerated axons.
Researchers discovered that a protein called HDAC5 plays a crucial role in triggering the regrowth of damaged nerve cells. By activating HDAC5, scientists hope to develop treatments that enhance axon regrowth and potentially restore sensation in nerve injuries.
Neurons from the retina connect to the brain first, controlling the abundance of a protein called aggrecan. This allows cortical neurons to get the best spots for connections once two weeks have passed. Understanding this mechanism could help repair damaged neural networks and develop regenerative therapies.
Researchers at McGill University discover that excessive axonal pruning, rather than cell body death, plays a crucial role in neurodegenerative diseases. Protecting axons from degeneration may be key to developing novel therapies for these conditions.
Researchers found that removing specific receptors affects brain boundary formation differently than expected, suggesting new molecules may be involved. This discovery sheds light on the neural network development and could lead to therapies and diagnostics for brain diseases.
Biologists at the University of California, San Diego have identified a quality check system for neurons that uses two proteins to detect and mark defective cells. The discovery could lead to remedies or drugs for human disorders such as horizontal gaze palsy with progressive scoliosis.
Researchers found that embryonic nerve cells use two versions of a signaling molecule to determine which end is the axon and which is the dendrite. This discovery could help improve therapies for spinal cord injuries and neurodegenerative diseases.
Researchers found that the presence of stationary power plants at synapses controls the stability of nerve signal strength, while rapid mitochondrial movement causes fluctuating signals. This discovery may advance our understanding of human neurological disorders such as Alzheimer's disease and Parkinson's disease.
A team of researchers at ETH Zurich used high-resolution microelectrode arrays to measure axonal signal speed, finding significant variations within the same neuron. The study challenges the long-held assumption that axonal signal conduction is purely digital.
Researchers identified a molecular program controlling neuronal output connection growth via mitochondrial capture. The LKB1-NUAK1 signaling pathway spurs axon branching, pointing to its potential role in developmental brain disorders like autism and schizophrenia.
Researchers at the University of Illinois at Chicago discovered that genetic mutations associated with inherited ALS can cause delays in nutrient and protein transport within nerve cells. This slowdown can lead to cell death, contributing to the neurodegenerative disorder.
A Weill Cornell study reveals that faulty wiring occurs when RNA molecules embedded in a growing axon are not degraded, interfering with new signals meant to guide the axon. This knowledge may lead to new therapies and strategies to correct faulty pathways.
Researchers discovered neurons employ distinct Caspase mechanisms for axon pruning and apoptosis, providing insights into neurological disorders. The study's findings shed light on the processes underlying neurodevelopmental disorders like schizophrenia and autism.
Researchers discovered a regenerative process involving damaged nerve fibers in the spinal cord that can improve functional recovery after stroke. The study found significant improvement in voluntary movement in mice whose axons were not severed, suggesting potential treatment targets for enhancing neurological recovery.
Researchers at WashU Medicine found a gene called Phr1 that governs the self-destruction of injured axons. Removing this gene can prevent axonal degeneration in adult mice, offering a potential target for new drugs to maintain nerve function.
Researchers identified a gene in the roundworm Caenorhabditis elegans that restricts the flow of cellular organelles from the cell body to the axon, potentially leading to neurodegenerative disorders. This discovery provides new insights into a previously unrecognized trafficking system that protects axons.
Researchers have identified a gene in fruit flies that, when mutated, blocks self-destruction of damaged axons, which could hold clues for treating motor neuron diseases like ALS. The preservation of this signaling mechanism from flies to humans suggests its importance and potential as a treatment strategy.
A key protein in Schwann cells is essential for normal interactions between nerve cells and Schwann cells, regulating the steps that lead to nerve regeneration. Deficiency of this protein may lead to chronic neuropathic pain, motivating the development of a small molecule drug to mimic its function.
Researchers at Drexel University have identified two key molecules involved in promoting nerve cell growth and branching after injury. By manipulating the expression of these molecules, they were able to induce longer and more branched axons, which is essential for restoring nerve function.
Scientists at the University of Nevada, Reno have found a new mechanism for guiding nerve growth that involves cell-death machinery. This discovery may lead to therapeutics designed to keep neurons alive after injury, potentially stimulating re-growth or sprouting new connections.
Researchers discovered that crippled mitochondria in Schwann cells lead to a toxic substance build-up, causing nerve damage and symptoms like numbness and pain. This finding may lead to new therapeutic strategies to treat peripheral neuropathies, including drugs that block toxin buildup.
Researchers from Plymouth University have identified the role of Merlin in regulating axon integrity, a key factor in peripheral neuropathy. This discovery could lead to effective drug therapies for patients with neurofibromatosis type 2 (NF2) suffering from peripheral neuropathy.
Researchers found that fragile X syndrome alters signaling in brain cells, leading to prolonged electrical surges and potential attention problems. Restoring the gene FMRP restored normal signaling.
Researchers at Max Planck Institute of Experimental Medicine found that peripheral glial cells produce neuregulin1 to support nerve repair and myelin regeneration. Neuregulin1 is essential for the maturation of Schwann cells and the regeneration of damaged nerves.
Researchers developed an oral drug that improved limb movement and preserved myelin-surfacing cells in mice after a spinal cord injury. The compound efficiently crossed the blood-brain barrier and showed no toxic effects, with the highest dose demonstrating significant improvements in motor function.
Researchers at Johns Hopkins Medicine have discovered a complex signaling system that directs nerve cell branching and connectivity, using protein signals like Sema-1a to coordinate axon travel patterns. This study has broad implications for human disease research, particularly in understanding muscle control and nerve disorders.