Researchers discovered that microglia's TGF-beta signaling acts as a brake, preventing nerve fibre damage in ageing spinal cords. This protective mechanism may contribute to the development of certain neurological diseases.
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A study among WTC responders with chronic PTSD found measurable physical changes in their brain structure, including cortical changes and imbalance of myelinated to unmyelinated neurons. These changes were most strongly associated with re-experiencing symptoms in individuals with PTSD.
The National Multiple Sclerosis Society has committed $18.1 million to support research projects aligned with its Pathways to Cures roadmap, which aims to stop MS, restore function, and end the disease. The funding includes 16 research grants and 28 training fellowships in the US and internationally.
A rodent study found hnRNP A1 regulates myelin production and maintains its integrity, suggesting an impact on neurodegenerative diseases like schizophrenia. The findings provide new insights into the disease's molecular basis and potential treatments.
A research group has uncovered a potential mechanism linking maternal inflammation to delayed neurodevelopment in infants. CD11c-positive microglia, crucial for myelination, play a key role in this process.
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Dr. Mikael Simons is being recognized for his pioneering research on myelin biology, glial cell biology, and neuroinflammation that continues to inform MS research. His work has helped identify a promising therapeutic target with potential to benefit people with MS.
Researchers at the Plasticity and Remodeling of Neural Circuits laboratory aim to stimulate myelin plasticity to regenerate affected nerve fibers in MS patients. The team will explore gene therapy, pharmacological approaches, and rehabilitation strategies to enhance myelin repair.
A new study published in The FEBS Journal found that protein C1QL1 plays a crucial role in promoting the replacement of specialized cells responsible for producing myelin. This discovery could lead to novel therapies for demyelinating diseases like multiple sclerosis.
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A new study found that 40Hz sensory stimulation preserves myelination, protects oligodendrocytes, and sustains electrical signal transmission in the brains of mice with cuprizone-induced myelin loss. The researchers also identified molecular mechanisms underlying these benefits.
Researchers have developed a new therapy called PIPE-307 that targets an elusive receptor on certain cells in the brain, prompting them to mature into myelin-producing oligodendrocytes. This could potentially reverse damage caused by multiple sclerosis, leading to improved movement, balance, and vision.
Researchers have discovered a small molecule compound called ESI1 that can regenerate vital myelin coatings, potentially treating multiple sclerosis and age-related cognitive deficits. The treatment promotes healing by clearing a roadblock in the repair process, allowing oligodendrocytes to produce myelin sheaths.
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Researchers found that ancient retroviruses are essential for myelin production in mammals, amphibians, and fish. The gene sequence RetroMyelin is likely a result of ancient viral infection, and its presence is necessary for myelination to occur.
Researchers at Tokyo Medical and Dental University develop a genome-editing technique that decreases PMP22 protein levels in patient cells, potentially reversing CMT-related changes. The study aims to improve myelination abilities and reduce symptoms in patients with CMT type 1A.
Researchers found an inverse relationship between axon loss and demyelination, suggesting that 'bad' myelin can be more damaging than its absence. This study identifies potential therapeutic targets for diseases associated with myelin defects and inflammation in the nervous system.
A new study suggests that hormonal birth control used by adolescents may influence the development of their brain, leading to altered risk assessment. The researchers found increased myelination and decreased immune cells in the brains of treated rats, while also exhibiting signs of impulsivity in behavior tests.
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Microglial cells age differently in male and female mice, with female microglia displaying a 'middle-aged' phenotype and male microglia switching suddenly to an aged phenotype. The researchers identified key genes and mechanisms contributing to this aging process, including the role of aged-like microglia in cognitive decline.
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 at Duke-NUS Medical School have identified a special transporter protein that regulates the formation of myelin sheaths in the brain, which protect nerves from damage. The study suggests that omega-3 fatty acid lipids play a crucial role in directing oligodendrocyte development, a process critical for brain myelination.
Researchers developed a novel tool to monitor recovery after CNS demyelination, enabling early testing of pro-remyelinating strategies. This new approach shows promising results in reducing clinical failure and advancing therapeutic success for multiple sclerosis.
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Researchers at UC Davis discovered how oligodendrocyte-lineage cells transfer cell material to neurons in the mouse brain, providing a new mechanism for understanding brain maturation and finding treatments for neurological conditions. This discovery opens new possibilities for treating neurodegenerative diseases like Alzheimer's and P...
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.
Researchers at Aarhus University are developing a novel treatment for multiple sclerosis by spinning artificial nerve fibers using electro-spun fibres. The goal is to restore nerve impulses quickly, as the myelin sheath deteriorates with age.
The APOE4 gene variant increases the risk of Alzheimer's disease by disrupting the insulation of brain wiring. Research found that oligodendrocytes mismanage cholesterol, failing to transport fat molecules to myelinate axons. This deficiency may contribute to the pathology and symptoms of Alzheimer's.
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Researchers at Massachusetts General Hospital have developed a radioactive demyelination tracer that can be detected by PET scans. The tracer was found to be safe and well-tolerated in healthy volunteers, but cleared from circulation faster than expected.
Researchers discover that neurons directly contribute to Krabbe disease destruction through enzyme galactosylceramidase. This finding presents a new approach to developing therapies for the rare neurodegenerative disorder.
Researchers found that myelination, even patchy on interneurons, is required for full inhibitory potential. Myelin loss can cause abnormal brain activity and lead to cognitive impairments.
Researchers found increased myelination in areas associated with emotions and memory in individuals with anxiety and PTSD, correlating with specific symptoms. This study provides a possible explanation for individual variation in stress response and may lead to targeted treatments.
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Scientists at Ann & Robert H. Lurie Children's Hospital of Chicago discovered a surprising link between growth factor receptor PDGFRA and hypomyelination in mouse models. The study suggests that blocking this receptor could be a novel strategy to treat myelination disorders like multiple sclerosis.
Researchers found that a new remyelinating drug called indazole chloride improved vision in mice with multiple sclerosis by inducing remyelination and mitigating damage to the optic nerve. The study highlights the importance of early treatment to mitigate axon damage and recover 75-80% of original function.
A research team identified a mechanism to control myelin sheath restoration after injury or in multiple sclerosis, regenerating damaged sheaths with theophylline. The study found significant recovery of myelin sheaths in both peripheral and central nervous systems, promoting efficient remyelination.
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A new study by University of Wisconsin-Madison researchers found that changes in VEP latency can accurately reflect remyelination in multiple sclerosis patients, providing a potential outcome measure for evaluating new treatments.
A study published in GLIA found that myelin impairment causes uncoordinated electrical impulse transmission between neurons, affecting motor learning in mice. The research also showed that compensating for impaired motor learning by pairing actions with brain photo-simulation can promote synchronization of neuronal activities.
Researchers found that children's brains are becoming more myelinated, which could affect estimates of cortical thickness. This discovery challenges previous hypotheses on brain development and has implications for understanding neurodegenerative diseases like Multiple Sclerosis.
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Researchers analyzed postmortem brain samples from 24 people with Alzheimer's and 24 without the disease to identify cellular pathways affected by the disease. The study found that axon myelination is disrupted in patients, and gene expression patterns vary significantly between men and women, suggesting potential new drug targets.
A study by MIT neuroscientists found that a genetic mutation linked to Williams Syndrome leads to thinning of the fatty layer that insulates neurons. Reversing this effect with drugs improved symptoms, suggesting a new direction for treatment.
B cells play a key role in helping neurons develop by stimulating axon myelination, suggesting a potential link between B cell dysfunction and neurodevelopmental disorders. The study found that specific B cell antibodies promote oligodendrocyte proliferation and neuron myelination.
Researchers developed a neutralizing agent for CSPGs that inhibit oligodendrocyte migration and differentiation. Protamine was found to inhibit CSPG-mediated inhibition of oligodendrocyte differentiation, enhancing myelination in the developing mouse brain and remyelination in adult mice.
A team of researchers from the University of Wisconsin-Madison reports that in long-lived animals, renewed but thin myelin sheaths are enough to restore the impaired nervous system. The findings confirm that thin myelin sheaths support nerve fiber function and survival, providing a potential marker for remyelination.
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A study by Osaka University researchers found that fibroblast growth factor 21 (FGF21) promotes remyelination in mice, suggesting a potential new treatment for demyelinating diseases. FGF21 was shown to increase remyelination and improve neurological function in mice with demyelinated lesions.
A new study published in PLOS Biology reveals that different firing patterns of neurons alter proliferation and differentiation of oligodendrocyte precursors, which provide insulation to neuronal axons. The findings suggest a complex interplay between neurons and non-neuronal cells supporting them.
Researchers at Boston Children's Hospital have identified a new cause of brain defects in tuberous sclerosis complex (TSC) patients. The study reveals that a protein called connective tissue growth factor (CTGF) impedes oligodendrocyte development and myelination in the brains of TSC patients.
New research reveals that low birth weight babies may develop motor and neurological deficits due to peripheral nerve defects. The study suggests delayed myelination of the peripheral nervous system as a contributing factor.
Researchers at Boston University School of Medicine have discovered a genetic risk factor for binge eating, linked to decreased myelination. The findings could lead to novel therapeutic treatments targeting eating behaviors.
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A new cell therapy product called DUOC-01 promotes faster axon remyelination in mice treated with a demyelinating chemical agent. The treatment also enhances the differentiation of oligodendrocyte progenitor cells, suggesting potential for neuronal repair and remyelination in patients with demyelinating diseases.
Researchers found that a novel combination of prebiotics, milk fat globule membrane (MFGM) and lactoferrin added to a DHA- and ARA-containing formula advanced overall brain development in piglets. The study suggests that myelination occurred at a faster rate in piglets fed the supplemented diet.
Researchers at George Washington University and Case Western Reserve University have discovered two drugs that effectively treat multiple sclerosis by reversing the immune system's attack on nerve insulation, leading to increased remyelination. The study found that miconazole and clobetasol can promote myelination and enhance repair of...
Researchers have discovered a way to keep remyelination going using an FDA-approved drug solifenacin, which boosts myelin synthesis and improves auditory function in mice with myelin-related disease. The study shows that targeting human oligodendrocyte progenitor cells with solifenacin promotes differentiation and myelin production.
Recent studies have shown that microglia-conditioned culture medium supports OPCs' survival and enhances their differentiation. The role of microglia in remyelination is complex and varies depending on the timing of disease progression. Microglia/macrophage activation can lead to poor remyelination in MS plaques lacking microglia.
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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.
A £425,000 study at Queen's University Belfast aims to discover how the immune system supports tissue repair in Multiple Sclerosis (MS). The research seeks to understand how ageing affects this process and potentially lead to new treatments for MS.
A study published in Cell Stem Cell highlights the possibility of reversing ageing in the central nervous system for multiple sclerosis (MS) patients. The age-associated decline of remyelination, a regenerative process, can be reversed using inflammatory cells from young mice.
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Researchers at WashU Medicine have developed a new technique to rapidly access brain landmarks, enabling better brain maps and insights into how the healthy brain works. The technique speeds up long-distance signaling by mapping myelination levels, shedding light on brain evolution and function.
Researchers at UTHealth have demonstrated that transplanting genetically modified adult stem cells into an injured spinal cord can help restore electrical pathways associated with movement. The new cells, called oligodendrocyte precursor cells, facilitate remyelination and increase behavioral recovery.
A novel mouse model of demyelinating disorder has been developed, revealing the critical role of gene ZFP191 in CNS myelination. The study found that mice with a mutation in ZFP191 exhibit severe deficiency in CNS myelination, leading to tremors and seizures.
Two Brown University faculty members are awarded federal funding to investigate brain development in infants and children with bipolar disorder. The research aims to identify biological and behavioral markers that distinguish between full-blown and sub-syndromal bipolar disorder, which could lead to more specific diagnoses and treatment.
Researchers at UCF create first lab-grown motor nerves with nodes of Ranvier, a breakthrough that could improve understanding of demyelinating conditions and enable new drug therapies. The team plans to use the model system to explore the origins of diabetic neuropathy and identify targets for new treatments.
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A University of Missouri study has disproven a long-held theory about the nervous system's development, identifying key proteins involved in the process. The findings shed light on how neurofilaments affect axonal diameters and could lead to a better understanding of neurological diseases such as multiple sclerosis.
Researchers identified an essential protein that plays a key role in myelination and remyelination, processes vital for healthy brain development and repair. The discovery has major implications for treating brain damage in newborns and may lead to treatments or interventions to enhance brain health.
Researchers propose a new mechanism for Alzheimer's disease, linking breakdown of myelin to amyloid-beta fibrils and neurodegeneration. Myelination is key to brain function, and its decline with age may underlie the disease's progression.
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Researchers discovered that astrocytes promote myelination by releasing leukemia inhibitory factor (LIF) in response to electrical impulses. This finding may lead to new treatments for demyelinating diseases, such as multiple sclerosis.