For the first time, scientists have developed a drug that completely reproduces the effects of physical recovery in stroke recovery, at least in mice. This finding, made by UCLA health researchers, could ultimately change the main causes of how we treat adult disabilities around the world.
The promising findings published in the journal Nature Communications identified a compound that triggers the same brain repair mechanism activated during traditional physical therapy, which may solve one of the most frustrating challenges in stroke recovery treatment.
“The goal is to have a drug that can be taken by stroke patients that can take rehabilitation effects,” said S. Thomas Carmichael, PhD, lead author of the study and chair of neurology at UCLA.
Anyone who has a loved one’s struggle through rehabilitation after hitting knows the hard nature of the process. Hour after hour of physical therapy, day after day, progress is usually small. For many patients, these needs prove overwhelming.
“The actual impact of recovery after stroke is limited because most patients cannot maintain the intensity of recovery required for stroke recovery,” Carmichael explained.
What makes this development particularly important is that there is no pharmacological choice in stroke recovery. Although drugs are filled with drugs that prevent strokes or limit their immediate damage, there is nothing currently available to help the brain heal.
“In addition, stroke recovery is not like most other medical fields where there are drugs that can treat the disease, such as cardiology, infectious diseases or cancer,” Carmichael noted. “Rehabilitation is a physical medicine approach that has been around for decades; we need to transfer rehabilitation to the age of molecular medicine.”
Disconnect the network
To understand how recovery can help stroke recovery, Carmichael’s team studied lab mice and human stroke patients. Their investigation reveals that what happens in the brain after a stroke is surprising.
Damage is not limited to areas directly affected by stroke. Brain cells away from the stroke site are disconnected from the network. It seems like the entire community of the brain cannot communicate with each other, even if they are not directly damaged.
Many of these missing connections involve a specific type of brain cell, called albumin neurons, the researchers found. These specialized cells help generate what scientists call “γ oscillations” – arrhythmic patterns that coordinate brain activity in neural networks.
Think of gamma oscillation as the conductor of a neural band to make everything harmonious. After the stroke, the commander disappeared and the symphony of his brain fell into chaos.
The UCLA team observed that successful recovery, both in mice and humans, repaired these gamma oscillations and repaired the lost link between mouse albumin protein neurons.
From mechanism to medicine
Once they understood this mechanism, the researchers identified two candidates designed specifically to stimulate albumin protein neurons, which had the potential to initiate natural repair processes in the brain.
When tested in a mouse model, a compound – a compound developed in the UCLA lab of Dr. Varghese John, who co-authored the study, which showed excellent results. Mice treated with this drug showed significant recovery in motor control, reflecting the benefits of intensive recovery.
Although these results are promising, it is important to note that additional studies are needed to evaluate the safety and effectiveness of the drug before starting a human clinical trial. The leap from mouse models to human therapy remains large, with many promising therapies failing to translate across species.
However, this finding represents a potential paradigm shift in stroke recovery. Rather than relying solely on physical rehabilitation (a physical rehabilitation that many patients cannot maintain the necessary intensity), it is better to say that one day drugs that directly stimulate the brain’s repair mechanism will be prescribed.
New hope for stroke survivors
The meaning is not just convenience. For millions of stroke survivors around the world, many of whom live in permanent disabilities due to inability to fully recover, the drug can bring new hope to restore lost functions.
Elderly patients who usually lack physical endurance for heavy density recovery may benefit from pharmacological approaches. Similarly, individuals in areas with limited access to rehabilitation services may receive more effective treatments.
The study also highlights how understanding the fundamental mechanisms of the brain lead to novel treatments. By identifying the role of albumin neurons and gamma oscillations in stroke recovery, scientists have identified potential targets for previously unrecognized interventions.
As researchers work to transfer this potential treatment from the laboratory to the clinic, stroke patients continue to rely on traditional rehabilitation. But maybe not long. If DDL-920 or similar compounds are effective in humans, stroke recovery may eventually join other medical fields where molecular medical supplementation even replaces physical interventions.
Currently, Carmichael and his team continue to investigate, hoping to unlock molecular symphony of brain repair and conduct it with drug accuracy, which certainly changes one of the most challenging conditions we treat medicine.
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