Good news!
"... Key takeaways
- ... researchers identified a loss of brain connections that stroke produces that are remote from the site of the stroke damage.
- ... team found that some of the connections lost after stroke occur in a cell called a parvalbumin neuron, which helps a brain rhythm function.
- The researchers found that a drug called DDL-920 ... produced significant recovery in movement control in mice.
...
team found that some of the connections that are lost after stroke occur in a cell called a parvalbumin neuron. This type of neuron helps generate a brain rhythm, termed a gamma oscillation, which links neurons together so that they form coordinated networks to produce a behavior, such as movement. Stroke causes the brain to lose gamma oscillations. Successful physical rehabilitation in both laboratory mice and humans brought gamma oscillations back into the brain and, in the mouse model, repaired the lost connections of parvalbumin neurons. ...
team then identified two candidate drugs that might produce gamma oscillations after stroke. These drugs specifically work to excite parvalbumin neurons.
The researchers found one of the drugs, DDL-920 ... produced significant recovery in movement control in mice.
This study has two major areas of impact:
First, it identifies a brain substrate and circuity that underlies the effect of rehabilitation in the brain.
Second, the paper then identifies a unique drug target in this rehab brain circuity to promote recovery by mimicking the main effect of physical rehab.
..."
From the abstract:
"Motor disability is a critical impairment in stroke patients. Rehabilitation has a limited effect on recovery; but there is no medical therapy for post-stroke recovery. The biological mechanisms of rehabilitation in the brain remain unknown.
Here, using a photothrombotic stroke model in male mice, we demonstrate that rehabilitation after stroke selectively enhances synapse formation in presynaptic parvalbumin interneurons and postsynaptic neurons in the rostral forelimb motor area with axonal projections to the caudal forelimb motor area where stroke was induced (stroke-projecting neuron). Rehabilitation improves motor performance and neuronal functional connectivity, while inhibition of stroke-projecting neurons diminishes motor recovery. ...
Pharmacological enhancement of parvalbumin interneuron function improves motor recovery after stroke, reproducing rehabilitation recovery. These findings identify brain circuits that mediate rehabilitation-recovery and the possibility for rational selection of pharmacological agents to deliver the first molecular-rehabilitation therapeutic."
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