Researchers at University of Cologne identify p35-mediated CDK5 hyperactivity as a central mechanism limiting nerve regeneration in diabetes. Targeted interventions using peptides restore nerve fiber growth, leading to significant motor and sensory improvements.
Researchers introduced a recombinant protein to pericytes, which change shape and create cellular bridges that support axon regeneration. In mouse experiments, the treatment promoted robust axon regenerative growth and restored leg function.
Researchers at HKUST established a pre-OPN OTI model to investigate functional axonal rewiring following CNS injury. They found that intrinsically photosensitive RGCs mediate functional recovery, and proposed a dual-intervention strategy to enhance regeneration efficiency
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A collaborative study led by HKUST sheds light on new possibilities for treating CNS injuries through the discovery of a novel gene regulating axon regeneration. Lipin1 inhibition promotes nerve repair and boosts regeneration in both motor and sensory axons after spinal cord injury.
Researchers at HKUST have discovered a neuroprotective mechanism involving microglia that prevents acute axonal degeneration after spinal cord injury. Microglia establish direct contact with myelinated axons, exhibiting a protective wrapping behavior that delays degeneration.
Researchers at University of Cologne discover Cnicin, a plant-based compound that significantly accelerates axon growth in animal models and human cells. This breakthrough has the potential to treat paralysis and neuropathy by enabling nerves to regenerate more quickly.
Researchers at CityU and HKUMed developed genetically modified human neural stem cells that promote neural circuit reconstruction, reduce glial scar accumulation, and enhance axon outgrowth. The therapy demonstrates potential for treating severe spinal cord injuries with functional recovery.
Glycosaminoglycans, complex sugars in the brain's extracellular matrix, regulate neural connectivity through sulfation patterns. This discovery could lead to treatments for neurodegenerative diseases and psychiatric disorders by manipulating these patterns.
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A team of researchers found that a small population of nerve cells exists in everyone that could be coaxed to regrow, potentially restoring sight and movement. The discovery provides new insights into how axons grow and could lead to effective therapies for blindness, paralysis, and other disorders caused by nerve damage.
Researchers have successfully used AAV1.NT-3 gene therapy to improve muscle physiology and prevent age-related sarcopenia in mice. The treatment resulted in restored muscle mass, strength, and neural connections, offering a potential new option for managing this debilitating condition.
A research team led by Dr. Eddie Ma Chi-him identified a therapeutic small molecule M1 that increases mitochondrial dynamics and sustains long-distance axon regeneration, restoring visual functions in mice. Regenerated axons elicited neural activities and survived for four weeks after optic nerve injury.
Researchers have identified an intrinsic immune mechanism that promotes axon regeneration in peripheral nerves after injury. Deleting PTPN2 and combining it with type II interferon IFNγ accelerates axon regrowth, a potential breakthrough for treating spinal cord injuries.
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Researchers developed an epigenetic activator TTK21 to aid spinal cord regeneration in mice 12 weeks after severe injury. Treatment improved axon sprouting, sensory axon growth, and halted retraction of motor axons, leading to potential breakthroughs for human patients.
Researchers at OIST Graduate University developed a new 3D scaffold design using 2-photon lithography that guides regenerating neurons in the right direction. The scaffolds promote directional growth of neurons, bridging gaps and repairing connections after spinal injuries.
Researchers at WashU Medicine identified a drug that helps sensory neurons regrow after spinal cord injury. The drug, fenofibrate, activated support cells and improved recovery by about twice as much as a placebo. This finding offers potential for repurposing an FDA-approved compound to restore sensory function.
Researchers found that a protein called CXCL12 attracts growing nerve fibers and keeps them entrapped at the injury site. This prevents regeneration in the central nervous system. Eliminating the receptor for CXCL12 improved axonal regeneration, offering a potential starting point for new drugs.
Researchers have identified 40 genes that suppress axon regeneration in central nervous system cells, hindering recovery from brain and spinal cord injuries. By editing out one gene, they restored axons in mouse models with glaucoma, suggesting a potential new approach to treating neural damage.
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Scientists have used gene therapy to regenerate damaged nerve fibers in the eye, potentially leading to new treatments for glaucoma. The technique stimulated regeneration and protected retinal neurons from cell death, offering hope for protecting vision loss.
Researchers at Temple University Health System have identified a new mechanism for promoting neuron regeneration after spinal cord injury, involving the metabolic switch associated with glucose metabolism in glial cells. The study found that upregulating glycolysis in glial cells can stimulate axon growth and improve functional recovery.
Biologists at the University of Bayreuth have discovered a unique form of rapid regeneration in zebrafish neurons. Mauthner cells, responsible for escape behavior, can regenerate their axons within a week after injury. This finding disproves the widely accepted view that these cells are unable to regenerate.
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Researchers from Indiana University School of Medicine discovered that boosting energy levels in damaged nerve fibers can promote axonal regeneration and functional recovery after spinal cord injury. Deleting a protein anchor in the mitochondria also improved motor functions.
Regulating lipid metabolism in neurons has been shown to promote axon regeneration, with triglyceride synthesis impeding and phospholipid synthesis promoting regrowth. This new direction for research may provide translational targets for CNS injury treatment.
Researchers have successfully regenerated human retinal ganglion cells in a laboratory dish using lessons learned from rodent models. The discovery could lead to new methods of screening for drugs and genes impacted by glaucoma, potentially offering hope for vision loss patients.
Researchers at Waseda University have found that inhibiting the phosphorylation of CRMP2, a microtubule-binding protein, suppresses degeneration and promotes regeneration of nerve fibers in the optic nerve after injury. This breakthrough could lead to the development of novel treatments for patients with optic neuropathies such as glau...
Researchers discovered that a muscle protein called LIM protein (MLP) can promote nerve healing by stabilizing structures in growth cones. Blocking or suppressing MLP's function reduces nerve cells' ability to grow axons.
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Researchers identified a suite of genes that must be turned off for axons to regenerate in peripheral nerves after injury. To regrow, neurons must transition back to an immature state and re-engage developmental programs. The study provides evidence for the idea that cells must become less mature to regenerate.
Scientists at Temple University Health System have identified LKB1 as a critical regulator of axon regeneration in mature neurons, leading to significant gains in functional recovery in mice with spinal cord injuries. Targeted upregulation of LKB1 protein stimulated long-distance neuron regeneration and improved locomotor function.
Data from Neuroscience 2018 presents genetic deletion of SARM1 protecting axons and reducing biomarkers of neurodegeneration. SARM1 inhibition provides critical insight into developing disease-modifying therapeutics for patients with axonal degeneration.
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Researchers have discovered a three-pronged recipe to regenerate severed nerve fibers across complete spinal cord injuries, replicating conditions that promote growth during development. The treatment involves delivering growth factors and proteins to reanimate the genetic program for axon growth and create a permissive environment.
Researchers at Nagoya University have identified a signaling cascade involved in the regeneration of damaged nerves in roundworms, which shares similarities with the recognition and engulfment of apoptotic cells. This discovery may lead to pharmaceutical interventions to treat conditions like brain and spinal cord injuries.
A Yale research team identified a gene that can spur regeneration of axons in nerve cells severed by spinal cord injury when eliminated. The study found over 580 genes potentially involved in regeneration, with one gene, Rab27, leading to successful axon regeneration in mice.
Scientists successfully grafted human neural progenitor cells into rhesus monkeys with spinal cord injuries, growing hundreds of thousands of human axons and synapses. The findings represent a major step toward future human clinical trials for paralyzing spinal cord injuries.
A new study found that a specific transcription factor can help certain neurons regenerate, but simultaneously kill others, in the optic nerve. This discovery may lead to new treatment strategies for restoring vision or repairing injury by regenerating functional connections and considering combination therapies.
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Chelating zinc has been shown to promote survival of neurons in the retina and stimulate repair of damaged nerve fibers. In a mouse model, researchers saw dramatic levels of axon regeneration after using zinc chelators.
Researchers studied nerve regeneration in roundworms and discovered a signaling pathway that induces nerves to regenerate. This pathway is also involved in clearing dying cells, suggesting a potential target for improving human recovery from nerve injury.
Researchers will investigate molecular and genetic factors guiding axon growth in the retina, with goals of restoring vision through neuronal regeneration. The projects aim to develop breakthrough therapies for blinding diseases such as age-related macular degeneration and glaucoma.
A biomedical engineer from the University of Houston is using a $1.2 million grant to develop technology platform for axonal regeneration in nervous system. The goal is to understand how shifts in chemical gradients affect axonal growth, with potential applications for neurodegenerative diseases and neural prosthetics.
A study in mice funded by the National Institutes of Health shows that high-contrast visual stimulation can help regenerate optic nerve fibers, allowing for partial restoration of visual function. The research demonstrates that adult regenerated central nervous system axons are capable of navigating to correct targets in the brain.
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Researchers found that aging diminishes the mammalian central nervous system's ability to regenerate axons after a spinal cord injury. As a result, middle-aged adults already have a significantly reduced ability to regenerate compared to young adults.
Researchers at UCLA found that nerve cells regrow better when glial scarring is left intact, challenging the assumption that scars impede regeneration. The study revealed that glial scars can actually stimulate axon growth and regeneration, leading to new approaches for repairing spinal cord injuries.
Researchers at Hong Kong University of Science and Technology found that enhancing neuronal activity through melanopsin and DREADD-Gq stimulates axonal regeneration in adult mice. This suggests a new approach to facilitate neural repair after CNS damage.
Frank Bradke's groundbreaking research on neural regeneration and spinal cord injuries has earned him the coveted Leibniz Prize. His work aims to promote axon regeneration after spinal cord injury, inhibiting scar tissue formation and activating nerve cells' regenerative potential.
Researchers have identified a mechanism that allows the nervous system to heal itself by correctly directing axons to reconnect. Using zebrafish with fluorescent proteins, they found that regenerating axons explore both correct and incorrect paths but are guided towards the proper direction by extracellular matrix components.
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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 at Boston Children's Hospital have identified previously unrecognized proteins and pathways involved in nerve regeneration using proteomics techniques. Adding back the oncogene c-myc achieved unprecedented optic nerve regeneration in mice, promoting survival and axon growth.
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.
Researchers have identified KLF transcription factors as key regulators of axon growth and regeneration in the central nervous system. The study found that these factors suppress axon regeneration in neurons, highlighting the complex genetic programs involved in this process.
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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.
A lack of standards for experimental design and reporting hinders progress in developing therapeutics for spinal cord injuries. Implementing data standards and ontologies can facilitate transparency and analysis in neural plasticity and regeneration.
Researchers investigate gene therapy as a potential treatment to improve viability and regenerative capacity of injured adult retinal ganglion cells. Studies using modified viral vectors introduce genes into injured visual pathway cells, aiming to promote long-distance axon regeneration.
Researchers discovered that dental pulp stem cells can protect retinal ganglion cells from death and promote regeneration of their axons. The study found that these stem cells naturally express neurotrophic factors, providing a potentially limitless source of growth factors for injured neurons.
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Researchers at Stowers Institute for Medical Research identify a critical developmental window of one week after birth for establishing proper olfactory neuron connections. After this period, regenerated neurons lose the capacity to make correct connections and may become mis-wired.
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 have discovered a novel approach to bridge the glial scar following chronic spinal cord injury using self-donated Schwann cells. This breakthrough enables regenerated and elongated brainstem axons to cross the bridge, potentially leading to improved hind limb movement in rats with spinal cord injury.
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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.
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 X-ray irradiation inhibits glial scar formation, promoting axonal regeneration and improving locomotor function. The optimal treatment time window is day 7 post-injury.
A gene called spastin plays a critical role in axon regeneration, which was found to be shut down by a mutation in the gene. The researchers used fruit flies as a model organism and observed that severed axons regrew normally when the gene was present.
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Researchers at WashU Medicine identified a protein called dual leucine zipper kinase (DLK) that regulates signals telling the nerve cell it's injured, allowing nerve regeneration. The study shows DLK governs whether the neuron turns on its regenerative program.