New neuronal pathway may carry Alzheimer's-related proteins between cells
Overview: Researchers report the discovery of microscopic, membrane-to-membrane links between neurons — which they call dendritic nanotubes — that can transmit electrical signals and shuttle larger molecules, including proteins associated with Alzheimer's disease.
What the study did
A team from the Johns Hopkins School of Medicine and the University of Tokyo Graduate School of Medicine published findings in Science (October 2025) after examining both mouse and human brain tissue using high-resolution electron microscopy. The technicians combined these observations with live experiments in cultured neurons to track how the structures form and function over time.
Key findings
Previously, many neuroscientists assumed that neurons communicated primarily via synapses, the specialized gaps that transmit chemical and electrical signals. The new study shows that some thin neuronal protrusions (formerly regarded as filopodia) instead form direct membrane-to-membrane connections between neighboring neurons. The authors call these links dendritic nanotubes.
Observed in both mouse and human samples and active in the visual cortex, the nanotubes appeared capable of:
- conducting electrical activity between cells, and
- transferring larger molecular cargo, including an Alzheimer’s-associated protein injected in experimental samples.
In controlled mouse-brain experiments, the injected protein spread from the targeted neuron to nearby neurons along these nanotube pathways. When researchers blocked nanotube formation experimentally, the protein's spread was halted — suggesting these structures can provide a direct route for disease-linked material in laboratory conditions.
Why it matters
This work offers the first detailed description of an alternative neuronal communication system that can carry both electrical signals and larger cargo. If dendritic nanotubes similarly operate in living brains, they could represent a mechanism that contributes to the cell-to-cell progression of toxic protein accumulation in neurodegenerative diseases such as Alzheimer's.
Caveats and next steps
Important caveats remain. The experiments demonstrating protein spread and its blockade were performed in mouse tissue samples and cultured neurons; the behavior of these structures in living human brains, the frequency of their occurrence, and their role across different brain regions and stages of disease require further study. Correlation is not causation — while the data support a plausible pathway for spread, they do not prove that dendritic nanotubes drive Alzheimer's progression in patients.
Future research will need to confirm how common dendritic nanotubes are in healthy versus diseased brains, whether they transport other pathogenic cargos, and whether safely targeting them could become a therapeutic strategy without disrupting normal neuronal function.
Context
Alzheimer’s disease is characterized by progressive memory loss and cognitive decline associated with abnormal protein accumulation and neuronal loss. Its precise causes are still not fully understood; epidemiological links exist between cardiovascular health, cognitive activity, and dementia risk. This discovery adds an important piece to the puzzle and opens new lines of inquiry for understanding and potentially intervening in early disease mechanisms.
Publication: Science (October 2025). Research teams: Johns Hopkins School of Medicine and University of Tokyo Graduate School of Medicine.
Bottom line: The identification of dendritic nanotubes provides a plausible cellular route for the transfer of Alzheimer’s-related proteins in laboratory settings and offers a promising, but still preliminary, target for future research into disease mechanisms and interventions.
