The permanent neurological deficits of multiple sclerosis patients largely depend on the extent of degeneration of long nerve fibers. The latter is initiated by ruptures in the cell membrane and the resulting influx of calcium ions. In Germany alone, more than 200,000 patients suffer from multiple sclerosis (MS). MS is an autoimmune condition and one […]Continue Reading ...
A 3D printed, two-millimeter implant (slightly larger than the thickness of a penny) used as scaffolding to repair spinal cord injuries in rats. The dots surrounding the H-shaped core are hollow portals through which implanted neural stem cells can extend axons into host tissues. Credit: Jacob Koffler and Wei Zhu, UC San Diego For the […]Continue Reading ...
Nerve cells stripped of their insulation can no longer carry vital information, leading to the numbness, weakness and vision problems often associated with multiple sclerosis. A new study shows an overlooked source may be able to replace that lost insulation and provide a new way to treat diseases like MS. Cells called neurons make the […]Continue Reading ...
Aug 29 2018 A study led by Ecole polytechnique fédérale de Lausanne in Switzerland has shed light on the biological mechanisms needed for nerve fibers to regenerate in spinal cord injury. Image Credit: Vshivkova / Shutterstock Using rat and mouse models of spinal cord injury, the researchers identified three components to the regeneration of axons […]Continue Reading ...
July 12, 2018 A team of bioengineers at UC San Diego has answered a question that has long puzzled neuroscientists, and may hold a key to better understanding the complexities of neurological disorders: Why are axons, the spindly arms extending from neurons that transmit information from neuron to neuron in the brain, designed the way […]Continue Reading ...
March 24, 2017 In lots of neurodegenerative stipulations — Parkinson’s illness, amyotrophic lateral sclerosis (ALS) and peripheral neuropathy amongst them — an early defect is the lack of axons, the wiring of the worried machine. When axons are misplaced, nerve cells can not keep up a correspondence as they must, and worried machine serve as […]Continue Reading ...
April 21, 2017 FINDINGS New examine by means of scientists on the Eli and Edythe Vast Heart of Regenerative Medication and Stem Mobile Analysis at UCLA overturns a long-standing paradigm about how axons — thread-like projections that attach cells within the fearful formula — develop all over embryonic building. The findings of the learn, led […]Continue Reading ...
One of the outstanding questions in neurodevelopment research has been identifying how connections in the brain change to improve neural function during childhood and adolescence. Now, results from a study in rats just reported by neuroscientists Heather Richardson, Geng-Lin Li and colleagues at the University of Massachusetts Amherst suggest that as animals transition into adolescence, […]Continue Reading ...
Neuroscientists at UCLA, Harvard University and the Swiss Federal Institute of Technology have identified a three-pronged treatment that triggers axons – the tiny fibers that link our nerve cells and enable them to communicate – to regrow after complete spinal cord injury in rodents. Not only did the axons grow through scars, they could also […]Continue Reading ...
July 14, 2017 Scientists within the Vollum Institute at OHSU have known an enzyme that performs a the most important position within the degeneration of axons, the threadlike parts of a nerve mobile that transmit indicators inside the anxious device. Axon loss happens in all neurodegenerative sicknesses, so this discovery may open new pathways to […]Continue Reading ...
July 14, 2017 Scientists within the Vollum Institute at OHSU have recognized an enzyme that performs a a very powerful position within the degeneration of axons, the threadlike parts of a nerve mobile that transmit indicators throughout the anxious device. Axon loss happens in all neurodegenerative sicknesses, so this discovery may open new pathways to […]Continue Reading ...
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