A new study in mice suggests the brain’s protective barrier does more than block harmful substances. It also delivers essential proteins from the body, a process that may break down early in Alzheimer’s disease and offer a new target for treatment.
Scientists have long viewed the blood-brain barrier as a protective wall that prevents harmful substances from entering the brain. But a new study suggests it plays a far more active role, selecting beneficial proteins from the bloodstream and delivering them to specific brain cells.
Researchers at the Gladstone Institutes in San Francisco say the discovery could open the door to a new approach to treating Alzheimer’s disease, by targeting processes outside the brain itself.
The blood-brain barrier is a network of specialised cells lining blood vessels that separates the brain from the rest of the bloodstream.
“For a century, we’ve treated the blood-brain barrier as a simple physical boundary protecting the brain from toxins,” said study leader Andrew Yang of the Gladstone Institutes.
But the findings challenge that long-held understanding.
“We’re finding that it’s an intelligent interface that plucks the right proteins in the blood, often from distant parts of the body, and delivers them to the right cell types in the brain,” Yang said.
The researchers used Nobel Prize-winning protein-labelling chemistry to track 861 proteins in mouse blood without altering their function.
After injecting the labelled proteins back into the mice, the team examined brain tissue to identify which had crossed the barrier.
The study was published in the journal Cell on 11 November. Yang was the senior author, while Haoyue Zhou from his laboratory was the first author.
Scientists from the University of California, San Francisco, the Buck Institute for Research on Ageing, the Hong Kong Center for Neurodegenerative Diseases, Hong Kong University of Science and Technology, and Emory School of Medicine also contributed to the research.
Of the 861 proteins examined, just 92 crossed the blood-brain barrier.
Most originated in distant parts of the body, particularly the liver.
According to the Gladstone Institutes, the barrier uses specialised receptors to identify and transport selected proteins, rather than allowing them to enter the brain randomly.
Once across, the proteins are delivered to different types of brain cell, suggesting a highly selective transport system.
The researchers identified apolipoprotein A1 (APOA1), a protein produced in the liver, as particularly significant.
They discovered that APOA1 crosses into the brain and reaches specialised cells called astrocytes, helping to maintain healthy connections between neurons.
The team then examined mice with a form of Alzheimer’s disease to investigate what happens when this protein delivery system fails.
When the barrier stopped transporting APOA1, the resulting shortage was linked to the loss of connections between neurons, behavioural changes and other early signs of the disease.
Crucially, the researchers found that the barrier stopped importing protective proteins such as APOA1 before it began allowing harmful substances to leak into the brain.
This suggests that a failure in the brain’s protein supply system could be an early feature of Alzheimer’s, potentially preceding the more widely recognised breakdown of the barrier.
In a separate experiment, mice genetically engineered to produce more APOA1 in their livers showed increased delivery of the protein to the brain and fewer signs of Alzheimer’s.
“Alzheimer’s disease may not start entirely inside the brain. It may start when the brain’s supply line from the body is severed,” Yang said.
The findings raise the possibility of treating Alzheimer’s by restoring the supply of protective proteins from elsewhere in the body, rather than focusing solely on the brain.
“If that’s right, we may be able to fight this disease from outside the brain, by restoring what the brain has lost,” Yang said.
The researchers identified three potential approaches:
“We now have a map of the proteins the brain needs from the body and the transport system that delivers them,” Yang said. “We are excited to translate this blueprint into new therapies for Alzheimer’s that work from the outside-in, and into next-generation blood-brain barrier shuttles to deliver powerful medicines into the brain.”
Despite the promising findings, the research remains at an early stage and has so far been conducted only in mice.
It is not yet known whether the same protein transport failures occur in people with Alzheimer’s or whether restoring the supply could prevent or slow the disease in humans.
The study also does not establish that a disrupted protein supply is the initial cause of Alzheimer’s. Yang presents this as a possibility rather than a proven conclusion.
Neither the study announcement nor the accompanying reporting describes a treatment currently in development or undergoing human trials.
Nevertheless, the discovery offers scientists a new avenue to investigate: whether protecting the brain’s supply of essential proteins from the body could help combat Alzheimer’s disease.
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