A new study that was published in the February 1st issue of PLoS One suggests that the tau protein, which is indicative of the fibrous tangles in the brains of Alzheimer’s patients, spreads from neuron to neuron, from one region to the other, resulting in severe dementia.
In the study, the researchers used genetically modified mice to have a human gene for abnormal tau protein in the frontal lobe, where tau is supposed to begin its accumulation. The brains were analyzed over a period of 22 months to map the protein’s spread. They discovered that tau spread to different regions of the brain across the synapses. These new clues might provide a way to stop the neurodegenerative disease from getting worse.
Karen E. Duff, a pathologist at the Columbia University Medical Center, in New York City, states that this follows what they see in the earliest stages of human Alzheimer’s disease. Scientists knew that the disease spread from one region in the brain to others, but brain scans and autopsies remained inconclusive.
The tau pathology starts in the entorhinal cortex, and spreads from there. An effective treatment, which would emulate how physicians treat cancer, would include early detection and some form of a new treatment at the early stage of the disease, when it’s most amenable to treatment. This also could indicate how other neurodegenerative diseases, like Parkinson’s, spread.
It could take up to five years to learn what the study’s real implications are and how to effectively stop the movement of the tau protein.
Reference: “Trans-Synaptic Spread of Tau Pathology In Vivo” by Li Liu, Valerie Drouet, Jessica W. Wu, Menno P. Witter, Scott A. Small, Catherine Clelland and Karen Duff, 1 February 2012, PLoS One.