A new study by UCLA Health has discovered what researchers say it is the first medicine to completely reproduce the effects of rehabilitation of physical stroke in model mice, after studies in humans.
The findings, published in Nature communicationsHe tried two candidate medications derived from his studies on the mechanism of the brain effects of rehabilitation, of which one resulted in a significant recovery in control of the movement after the stroke in the mouse model.
The stroke is the main cause of adult disability because most patients do not recover completely from the effects of stroke. There are no medications in the field of recovery of the stroke, which requires that patients with strokes undergo physical rehabilitation that has proven to be modestly effective.
“The objective is to have a medicine that patients with stroke can take that produce the effects of rehabilitation,” said Dr. S. Thomas Carmichael, main author of the study and professor and president of UCLA Neurology. “Rehabilitation after stroke is limited in its real effects because most patients cannot maintain the necessary rehabilitation intensity for the recovery of stroke.
“In addition, the recovery of stroke is not like most other fields of medicine, where medications are available that treat the disease, such as cardiology, infectious diseases or cancer,” said Carmichael. “Rehabilitation is a physical medicine approach that has existed for decades; we need to move rehabilitation to an era of molecular medicine.”
In the study, Carmichael and his team sought to determine how physical rehabilitation improved brain function after a stroke and if they could generate a medication that could produce these same effects.
Working in laboratory mice stroke models and with patients with stroke, UCLA researchers identified a loss of brain connections that produces a stroke that are away from the site of the damage due to stroke. The brain cells that are located at a distance from the race site are disconnected from other neurons. As a result, brain networks do not shoot for things like movement and march.
The UCLA team discovered that some of the connections that are lost after the stroke occur in a cell called Parvalbumin neuron. This type of neuron helps to generate a cerebral rhythm, called gamma oscillation, which unites neurons to form coordinated networks to produce behavior, such as movement. The stroke causes the brain to lose gamma oscillations. Successful rehabilitation in both laboratory mice and humans brought gamma oscillations to the brain, and in the mouse model, repaired the lost connections of Parvalbumin neurons.
Carmichael and the team identified two candidate drugs that could produce gamma oscillations after stroke. These drugs work specifically to excite Parvalbumin neurons. The researchers found one of the drugs, DDL-920, developed in the UCLA laboratory of Dr. Varghe John, who co-author of the study, produced a significant recovery in the control of the movement.
More studies are needed to understand the safety and effectiveness of this medication before it can be considered for human trials.