FAU researchers identify microscopic cell tunnels that spread toxic proteins in Huntington’s disease

Researchers identify "tunneling nanotubes" as the secret pathway for Huntington’s disease spread, uncovering a new druggable target to halt toxic protein transfer.

By: AXL Media

Published: Mar 21, 2026, 5:43 AM EDT

Source: Information for this report was sourced from Florida Atlantic University

Uncovering the Infrastructure of Neurodegeneration

Huntington’s disease is a fatal brain disorder characterized by the accumulation of a toxic mutant protein that inevitably leads to the death of neurons. While researchers have long understood that this harmful protein spreads between cells, the physical mechanism of this transmission remained a significant biological mystery. A major breakthrough led by Florida Atlantic University has now identified "tunneling nanotubes"—microscopic, tube-like bridges—as the primary highways used by the disease to infect neighboring healthy cells.

The Rhes and SLC4A7 Protein Partnership

The study reveals that a specific protein already linked to the disease, known as Rhes, collaborates with an unexpected partner called SLC4A7. Historically recognized for its role in regulating cellular acidity, SLC4A7 was found to physically bind with Rhes at the cell membrane to trigger the growth of these nanotubes. This partnership essentially assembles the machinery required for cells to hand-deliver toxic material to one another, fundamentally changing the scientific understanding of how the disease moves through the brain’s architecture.

Direct Hand Delivery of Toxic Proteins

Unlike traditional cellular communication, which involves chemical signals diffusing through the space between cells, tunneling nanotubes allow for the direct transfer of physical cargo. While this sharing mechanism can help healthy cells manage stress, in the context of Huntington’s, it becomes a dangerous conduit for mutant huntingtin proteins. The research demonstrates that these nanotubes act as direct physical bridges, allowing the disease to bypass the normal boundaries of the cell and spread damage with high efficiency.