First-Ever Drug to Repair Brain Damage Caused by Stroke

A recent study by UCLA Health has identified what researchers believe to be the first drug that completely replicates the effects of physical stroke rehabilitation in mouse models, building on findings from human studies (1^✔ ✔Trusted Source
Parvalbumin interneurons regulaterehabilitation-induced functional recoveryafter stroke and identify arehabilitation drug

Go to source). The findings, published in Nature Communications, tested two candidate drugs based on research into the brain mechanisms involved in rehabilitation. One of these drugs led to significant recovery of movement control after a stroke in the mouse model.

Stroke is the leading cause of adult disability, as most patients do not fully recover from its effects. There are no specific drugs for stroke recovery, so patients rely on physical rehabilitation, which has shown only limited effectiveness.

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Challenges in Stroke Rehabilitation

“The goal is to have a medicine that stroke patients can take that produces the effects of rehabilitation,” said Dr. S. Thomas Carmichael, the study’s lead author and professor and chair of UCLA Neurology. “Rehabilitation after stroke is limited in its actual effects because most patients cannot sustain the rehab intensity needed for stroke recovery. Further, stroke recovery is not like most other fields of medicine, where drugs are available that treat the disease—such as cardiology, infectious disease or cancer,” Carmichael said. “Rehabilitation is a physical medicine approach that has been around for decades; we need to move rehabilitation into an era of molecular medicine.”

In the study, Carmichael and his team aimed to understand how physical rehabilitation enhances brain function after a stroke and whether they could develop a drug to replicate these effects.

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Impact of Stroke on Brain Networks

Working with both laboratory mice models and stroke patients, the UCLA researchers discovered that strokes cause a loss of brain connections far from the damage site. Brain cells located away from the stroke’s impact become disconnected from other neurons, preventing brain networks from firing together, which affects functions like movement and gait.

The UCLA team discovered that some of the connections lost after a stroke occur in a type of cell called a parvalbumin-positive positive neuron. These neurons play a key role in generating a brain rhythm known as gamma oscillations, which link neurons together to form coordinated networks necessary for behaviors like movement. A stroke disrupts gamma oscillations in the brain. However, successful rehabilitation in both laboratory mice and humans restored gamma oscillations, and in the mouse model, it also repaired the damaged connections in parvalbumin-positive neurons.

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Identifying Candidate Drugs for Stroke Recovery

Carmichael and team then identified two candidate drugs that might produce gamma oscillations after stroke. These drugs specifically work to excite parvalbumin-positive neurons. The researchers found one of the drugs, DDL-920, developed in the UCLA lab of Dr. Varghese John, who coauthored the study, produced significant recovery in movement control.

Further studies are needed to understand the safety and efficacy of this drug before it could be considered for human trials.

In conclusion, this study reveals the potential of DDL-920 to replicate the effects of physical stroke rehabilitation by restoring gamma oscillations and improving movement control in mice. While further research is needed, this breakthrough could lead to a new era in stroke recovery beyond traditional methods.

Reference:

1. Parvalbumin interneurons regulaterehabilitation-induced functional recoveryafter stroke and identify arehabilitation drug - (https://www.nature.com/articles/s41467-025-57860-0.epdf)

Source-Medindia