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Lyon, 9 March 2021 - Theranexus, a biopharmaceutical company innovating in the treatment of neurological diseases and pioneer in the development of drug candidates modulating the interaction between neurons and glial cells, today announced that it has extended the capabilities of Neurolead, its drug candidate discovery platform, to include autophagy and neurological manifestations of lysosomal storage disorders.
Neurolead, which combines the latest innovations in neuroscience and artificial intelligence, is a platform for the generation of new drug candidates based on a unique concept, the therapeutic targeting of interactions between glial and neuronal cells. By applying Neurolead to autophagy and neurological forms of lysosomal storage disorders, Theranexus is taking its research in the direction of exploring a therapeutic avenue of major interest with clear medical and economic potential.
Traumatic brain injury (TBI) is a major cause of disability and a risk factor for early-onset dementia. The injury is characterized by a physical insult.
Scientists receive the Brain Prize for groundbreaking contributions to novel migraine therapies
What:
The Brain Prize has been awarded to Michael A. Moskowitz, M.D., a professor of neurology at Harvard Medical School at the Massachusetts General Hospital, Charlestown, who also is supported by an NIH grant.
The Brain Prize is the world s most prestigious award for brain research and is awarded by the Lundbeck Foundation, Denmark. Dr. Moskowitz will receive the prize along with three other scientists for their pathbreaking contributions that led to novel migraine therapies.
The Lundbeck Foundation said, Moskowitz showed in experimental models that a migraine attack is triggered when trigeminal nerve fibers release neuropeptides that lead to dilated (opened up) blood vessels of the meninges, inflammation, and pain.. He was the first to propose that blocking the action of released neuropeptides could be a new approach to treating migraine.
Study shows how mutant huntingtin protein triggers brain cell death
In 1993, scientists discovered that a single mutated gene, HTT, caused Huntington s disease, raising high hopes for a quick cure. Yet today, there s still no approved treatment.
One difficulty has been a limited understanding of how the mutant huntingtin protein sets off brain cell death, says neuroscientist Srinivasa Subramaniam, Ph.D., of Scripps Research, Florida.
In a new study published in
Nature Communications on Friday, Subramaniam s group has shown that the mutated huntingtin protein slows brain cells protein-building machines, called ribosomes.
The ribosome has to keep moving along to build the proteins, but in Huntington s disease, the ribosome is slowed. The difference maybe two, three, four-fold slower. That makes all the difference.