There's a bouncer in everyone: the blood-brain barrier, a specialized layer of cells nestled between blood vessels and the brain's delicate tissues, vigilantly ejects toxins, pathogens, and other harmful agents that pose a threat to the brain's precious gray matter. However, when this vigilant ga
Researchers have discovered a therapeutic molecule, L6-F4-2, that enhances the blood-brain barrier’s strength by targeting the WNT signaling pathway. This breakthrough can potentially treat a variety of neurological disorders rooted in blood-brain barrier dysfunction, such as Alzheimer’s, multiple sclerosis, and brain tumors.
Methods of repairing the blood-brain barrier remain understudied, according to Kuo. But a recent paper he and colleagues led describes a treatment that could be instrumental in restoring the barrier’s normal function. Kuo is the senior author of the paper, recently published in“We have evaluated a new therapeutic class of molecules that can be used to treat a leaky blood-brain barrier; previously, there were no treatments directed at the blood-brain barrier specifically,” Kuo said.
Scientists have been focusing on frizzled, a protein receptor that initiates the WNT pathway, for blood-brain barrier therapies since mouse mutations in the frizzled gene cause blood-brain barrier abnormalities.Many different molecules bind to frizzled protein receptors, so to narrow their search for a potential therapeutic molecule, the researchers selected only those that specifically target cells that line the brain’s blood vessels.
The blood-retinal barrier performs the same function for the eye as the blood-brain barrier does for the brain. In Norrie disease, the development of blood vessels of the retina — the layer of light-sensitive cells in the back of the eye — is hindered, resulting in leaky blood vessel connections, improper development, and blindness.
Next, the researchers wanted to study a more common human condition — ischemic stroke (in which blood vessels and the blood-brain barrier are damaged, and fluid, blood, and inflammatory proteins involved in cellular communication can leak into the brain. They found that L6-F4-2 reduced the severity of stroke and improved survival of mice compared with mice that had untreated strokes. Importantly, L6-F4-2 reversed the leakiness of brain blood vessels after stroke.
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