Toxic protein spreads through the brain in patients with Alzheimer’s disease.
New research from Columbia University Medical Center indicates the toxic protein that causes Alzheimer’s disease literally jumps from one nerve cell in the brain to another.
Alzheimer’s disease typically affects only one area of the brain in the early stages. As the disease progresses, however, multiple areas are affected. Scientists have been unable to determine how the disease spreads.
A protein known as tau helps the brain’s nerve cells move nutrients and other substances. In patients with Alzheimer’s, the tau collapses into twisted strands, or tangles, and the transport system disintegrates.
Jessica Wu, PhD, and a former post-doctoral researcher at the Taub Institute who is currently at Massachusetts Institute of Technology, and colleagues tracked the movement of tau from one neuron to another. They found that damaged tau can be released from a neuron and move into the spaces between cells. Another neuron can then pick up the tau and seed other regions of the brain with Alzheimer’s disease.
“By learning how tau spreads we may be able to stop it from jumping from neuron to neuron,” co-author Karen Duff, PhD, said in a press release. “This would prevent the disease from spreading to other regions of the brain, which is associated with more severe dementia.”
Dr. Duff is a professor in the department of pathology and cell biology in the Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, and professor of psychiatry at New York State Psychiatric Institute.
The study also found that tau spreads faster when neurons are more active. Team members Abid Hussaini, PhD, and Gustavo Rodriguez, PhD, stimulated neurons in the brains of mice. The tau spread more quickly and lead to more damage in the neurons.
Trials in mice may or may not be relevant to how tau works in humans, but Dr. Duff said “they suggest that clinical trials testing treatments that increase brain activity such as deep brain stimulation should be monitored carefully in people with neurodegenerative diseases.”
The study was published in the June issue of Nature Neuroscience.
The study did not receive outside funding and none of the authors reported a conflict of interest.