Scientists at Johns Hopkins Medicine have discovered that mammalian brain cells can form microscopic tubes that transport toxic molecules between neurons, functioning like tiny “pneumatic tubes” within the brain. This process, observed in experiments using genetically engineered mice, helps explain how harmful proteins linked to Alzheimer’s disease might spread from one cell to another. The study, funded by the National Institutes of Health and published on 2 October in Science, could change how researchers think about the brain’s internal communication systems and open new directions for treating neurodegenerative disorders.
In their experiments, the researchers found that neurons form slender channels called nanotubes to remove small toxic molecules. One of them is amyloid-beta, a sticky protein that forms plaques that mark Alzheimer’s disease. Hyungbae Kwon, an associate professor of neuroscience at Johns Hopkins, explained that while these tubes help cells expel toxins, they also facilitate their spread. “Cells have to get rid of toxic molecules,” Kwon said, “but by producing a nanotube, they can transmit this toxic molecule to a neighbouring cell. Unfortunately, this also spreads harmful proteins through the brain.”
Using high-powered microscopes and live-cell imaging, the team watched neurons extend long, finger-like projections that connected one cell’s dendrites — the branch-like arms — to another’s. These structures, named dendritic nanotubes, acted as highways for transporting small molecules, calcium, and even toxic proteins. The researchers noted that the shape and flexibility of the tubes enabled them to rapidly transfer information and materials between cells that were not directly touching, revealing a form of communication previously hidden from scientists.
To explore this process further, the team built computer models to simulate how nanotubes contribute to the buildup of amyloid-beta early in Alzheimer’s disease. Their findings showed that the brain may have an extra “connectivity layer” of nanotubes that works alongside synapses — the traditional communication points between neurons. This suggests that the brain’s internal network is more physically linked than previously thought, and that these nanotubes might play a role in both maintaining and disrupting brain health.
The researchers examined brain tissue from healthy mice and from mice genetically modified to develop Alzheimer ‘s-like plaques. They discovered that diseased mice had more nanotubes at 3 months of age, before symptoms appeared, than healthy mice. By six months, the difference between the two groups had lessened. This pattern suggests that nanotube formation increases during the early stages of disease, possibly facilitating the rapid transport of toxic proteins through brain tissue. When the scientists studied human brain samples using publicly available electron microscopy data, they found nanotubes forming between neurons, a pattern similar to that observed in mice, suggesting that this mechanism exists in both humans and mice.
Kwon and his team now plan to test whether other brain cells, such as glial cells, also form nanotubes. They hope to learn whether controlling the creation of these tubes could help prevent or slow diseases like Alzheimer’s. If researchers can find a way to adjust nanotube formation — increasing it to remove waste or reducing it to stop the spread of toxins — they might one day use this discovery to protect brain cells from degeneration. This new understanding of how the brain moves molecules around adds an intriguing piece to the puzzle of how neurodegenerative diseases begin and progress. It offers hope for more targeted, effective treatments in the future.
More information: Hyungbae Kwonet al, Intercellular communication in the brain through a dendritic nanotubular network, Science. DOI: 10.1126/science.adr7403
Journal information: Science Provided by Johns Hopkins Medicine
