I would love to see this in human clinical trials.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=123207&CultureCode=en
New Research Published in Restorative Neurology and Neuroscience
In a study published in the current issue of Restorative Neurology and Neuroscience
scientists report that a therapy combining exercise with the
neurovascular protective agent S-nitrosoglutathione (GSNO) improved
recovery from stroke in a rat model. GSNO is a compound found naturally
in the body and it has no known side effects or toxicity.
“In our study, GSNO or motor exercise provided neuroprotection,
reduced neuronal cell death, maintained tissue structure, and aided
functional recovery by stimulating the expression of neuronal repair
mediators,” says lead investigator Avtar K. Singh, MD, of the Medical
University of South Carolina (MUSC) and the Ralph H. Johnson VA Medical
Center, Charleston. “GSNO in combination with exercise accelerated the
rate and enhanced the degree of recovery.”
Stroke is both an acute disease and a chronic condition. While the
acute phase is associated with cell death and secondary injury, the
chronic phase is characterized by insufficient neurorepair mechanisms.
Most monotherapies fail because the drugs are not effective in the
chronic phase. Rehabilitation has been used to improve neurofunction in
the chronic phase, but its efficacy is slow and limited. An ideal
therapy would ameliorate the injury in both phases and therefore include
a combination of rehabilitation and an agent that provides both
neuroprotection and repair, such as GSNO.
Dr. Singh and her colleagues from MUSC (Drs. Mushfiquddin Khan,
Harutoshi Sakakima and Inderjit Singh) induced stroke in rats, which
were then assigned to one of five treatment groups. The first group
received no treatment; the second group was treated with exercise; the
third group with GSNO; the fourth group received both exercise and GSNO
treatment; and the fifth group received a sham treatment. In the
exercise treatment, rats were required to run on a rotating rod motor
unit at a constant speed for 20 minutes a day. GSNO was administered
throughout the treatment period.
Animals in each group were evaluated for neurological function, motor
behavior, and locomotor function before and after the procedure. The
size of the infarct was measured. At 7 and 14 days after stroke was
induced, brain tissue samples were removed and tested.
Administration of GSNO not only reduced brain injury but also
improved neurological scores. Exercise alone could not significantly
reduce infarct volume, because the exercise started 72 hours post
procedure and infarctions occur before then. However, exercise did
improve neurobehavioral functions. Combining the therapies had a
synergistic effect, and provided greater functional improvement than
either GSNO or exercise alone.
Analysis of the brain tissue found that GSNO accelerates the recovery
of neurological and motor functions and enhances the benefit of
exercise by stimulating the expression of neurotrophic factor BDNF and
its receptors, which play critical roles in neurorepair processes, and
by activating Akt, a protein involved in cell proliferation. Dr. Singh
and her collaborators Drs. Mushfiquddin Khan and Inderjit Singh
conclude, “GSNO is an attractive candidate to be investigated in humans
for neurorepair and rehabilitation following stroke.”
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