Writing in a paper published on Wednesday, 04 December 2019, in the journal Science Translational Medicine, a group of researchers from the University of California (UC), Berkeley, and Ben-Gurion University report a breakthrough in the treatment of dementia.
According to the researchers, the aging brain is commonly treated as a simple case of neurodegeneration, whereby loss of function and the accumulation of dead cells lead to slowly decreasing performance in both higher cognitive and daily tasks.
And yet, as the study shows, once the “fog” of inflammatory load is lifted, “the aged brain acts like a young brain. It is a really, really optimistic finding, in terms of the capacity for plasticity that exists in the brain. We can reverse brain aging”, said senior author Professor Daniela Kaufer at UC Berkeley.
As was demonstrated in previous research, as the blood protein albumin crosses the blood-brain barrier (BBB) in response to head trauma or regular aging, it causes a cascade of cell death which, in turn, leads to cognitive decline in both humans and other animals.
When researchers genetically engineered mice so they could knock out the TGF-β receptor in brain cells called astrocytes which albumin binds to, after they’d reached old age, the brains of these mice were found to be comparable to those of young ones in terms of overall function.
Repairing the blood-brain barier might lead to the slowing down or even reversal of dementia and certain other neurodegenerative conditions. Image: Geralt via needpix.com
Another piece of evidence came with a drug, called IPW, which blocks the TGF- β receptor in astrocytes only, synthesized by a medicinal chemist Barry Hart at Palo Alto, California. When mice were given doses if IPW that lowered the receptor activity to that found in young mice, the brains of the aged mice looked younger, too.
This provides a tremendous amount of evidence for the radical hypothesis that dementia and many other neurodegenerative conditions might be caused by a leaky BBB. When analyzing human brain tissue, Kaufer and her colleagues found evidence of higher albumin concentrations in aged brains, which they then correlated with increased BBB leakiness by deploying a specially designed type of MRI imaging.
Co-authors Daniela Kaufer and Aaron Friedman, as well as Barry Hart, have now started a company to develop a drug for treating the BBB, which they hope to make available for clinical applications as soon as possible.
Source: paper, news.berkeley.edu