Spinal Muscular Atrophy Press Releases
New members selected for National Advisory Neurological Disorders and Stroke Council
Thursday, Jan 29, 2015
Five prominent individuals from the neuroscience community have joined the National Advisory Neurological Disorders and Stroke Council, the principal advisory body to the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health.
Spinal Muscular Atrophy May Also Affect Sensory Neurons
Thursday, Jun 2, 2011
Until recently, most researchers thought that problems with spinal muscular atrophy (SMA) began exclusively in motor neurons, the cells that transmit signals from the spinal cord to muscles. New results suggest for the first time that SMA may also affect sensory neurons, the cells that transmit movements and sensations to the spinal cord.
National Advisory Neurological Disorders and Stroke Council Welcomes Six New Members
Thursday, Feb 3, 2011
The NINDS announced that six new members have joined its National Advisory Neurological Disorders and Stroke Council, the Institute’s principal advisory body regarding research program planning and priorities. The new members are Ben A. Barres, PhD, Robert B. Darnell, MD, PhD, Sharon E. Hesterlee, PhD, Eve Esther Marder, PhD, Robert Enrico Pacifici, PhD, and Amita Sehgal, PhD.
NINDS Names Dr. Petra Kaufmann Director of the Office of Clinical Research
Wednesday, Sep 9, 2009
The National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health, has named Petra Kaufmann, M.D., M.Sc., as director of its Office of Clinical Research.
NIH Symposium Explores Promise of Stem Cell Therapies
Monday, Jul 14, 2008
Stem cells have been hailed as a toolkit to treat a host of diseases, but at an NIH symposium on May 6, researchers said they are still deciphering the toolkit’s instruction manual.
Blood-Clotting Protein Could be a Target for Therapy against MS
Monday, May 14, 2007
In multiple sclerosis (MS), the immune cells that patrol our blood for pathogens venture out of the bloodstream and attack the brain. Researchers have found that leakage of a blood-clotting protein into the brain, once considered merely a sign of damage in the MS brain, helps stimulate this attack.
Treatment Extends Survival in Mouse Model of Spinal Muscular Atrophy
Thursday, Feb 22, 2007
Drug therapy can extend survival and improve movement in a mouse model of spinal muscular atrophy (SMA), new research shows. The study, carried out at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS), suggests that similar drugs might one day be useful for treating human SMA.
Neurons Grown From Embryonic Stem Cells Restore Function In Paralyzed Rats
Tuesday, Jun 20, 2006
For the first time, researchers have enticed transplants of embryonic stem cell-derived motor neurons in the spinal cord to connect with muscles and partially restore function in paralyzed animals. The study suggests that similar techniques may be useful for treating such disorders as spinal cord injury, transverse myelitis, amyotrophic lateral sclerosis (ALS), and spinal muscular atrophy. The study was funded in part by the NIH’s National Institute of Neurological Disorders and Stroke (NINDS).
Pain Reliever May Provide Clues for Treating Spinal Muscular Atrophy
Thursday, Mar 3, 2005
New research suggests that an off-the-market pain reliever called indoprofen may be a starting point for finding a new drug to treat spinal muscular atrophy (SMA), a devastating childhood neurological disorder.
Valproic Acid Shows Promise for Treating Spinal Muscular Atrophy
Wednesday, Feb 18, 2004
Study Identifies Gene That Prevents Nerve Cell Death
One of the first studies of valproic acid as a potential therapy for spinal muscular atrophy (SMA) shows that, in cultured cells, the drug increases production of a protein that is reduced or missing in people with the disorder. While preliminary, the study suggests that valproic acid or related drugs may be able to halt or even reverse the course of this devastating childhood disease.
Friday, Oct 25, 2002
Many neurological diseases occur when specific groups of neurons die because of nerve damage, toxins, inflammation, or other factors. A new study suggests that activity of a single gene can stop neurons from dying regardless of what triggers this process. The findings could lead to new ways of treating neurodegenerative diseases.