Jumpstarting brain repair: promising stem cell therapy for ischemic stroke
A stem-cell therapy has demonstrated promise for ischemic stroke treatment, offering potential advantages over current conventional options.
In a recent study, researchers at the Gladstone Institutes (CA, USA) highlighted the transformative potential of SB623, a stem cell therapy for ischemic stroke. SB623 is an allogeneic modified bone marrow-derived human mesenchymal stem cell therapy developed by regenerative medicine company SanBio (Tokyo, Japan) and is currently in clinical development for the treatment of chronic motor deficits following traumatic brain injury and cerebral ischemic stroke.
Ischemic stroke is a leading cause of neurological disability in adults, with only about 5% of patients achieving full recovery. Most patients who do not fully recover face long-term disabilities, including motor disorders, chronic pain and epilepsy. While treatments like neurorehabilitation and acute thrombolytic therapy can aid recovery, they are most effective within hours of the stroke. Over time, the brain’s ability to heal slows, particularly in the area surrounding the injury, and brain activity changes.
Jeanne Paz, who led the research, and her team have been examining neurological changes that follow a stroke and the associated long-term effects. They previously found that cells in damaged brain regions can become hyperexcitable, sending overly strong or frequent signals to other brain regions, contributing to mobility issues and seizures.
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In their latest study, working alongside SanBio, the researchers at Gladstone Institutes investigated the effects of SB623 on brain excitability, brain tissue and peripheral blood at a chronic stage after ischemic stroke. SB623 has previously demonstrated significant therapeutic potential, including improvements in motor, however, the precise mechanism of action remains unclear. Understanding this mechanism could aid in future clinical trials.
To get an insight into how SB623 works, the team used a rat model of stroke. They injected SB623 , one month post stoke, into the area of the rats’ brain damaged by the stroke. One week after treatment, they conducted ex vivo assessments of cortical excitability. The therapy was found to reduce stroke-induced cortical hyperexcitability, restoring cortical activity to normal levels. Furthermore, increased levels of proteins and cells important for brain function and repair were observed.
These findings suggest that SB623 was able suppress hyperexcitability caused by ischemic stroke damage and, in the words of the researchers, helps “jump-start” the brain’s repair process after a prolonged period. This new understanding of the therapy’s mechanism could lead to potential applications for hyperexcitability-related neurological conditions.
Interestingly, the therapy had other positive effects. After analyzing blood samples from the rats, the researchers found that the therapy restored a specific combination of molecules involved in inflammation and brain health to normal levels, which had been altered by the stroke.
While SB623 demonstrated therapeutic potential, further research is needed to determine if reducing hyperexcitability addresses the long-term symptoms of ischemic stroke. The team is also seeking to understand how the stem cells may enhance brain function, potentially identifying key molecules for developing small-molecule drugs to replicate the effects of the stem cells.
SB623 has already been approved in Japan for improving chronic motor paralysis following traumatic brain injury. SanBio is also pursuing regulatory approval from the US Food and Drug Administration (MD, USA) and exploring additional indications for its use.
