University of Virginia neuroscientists have revealed how a toxic form of tau protein, notorious for forming tangles in the brains of people with Alzheimer’s disease and several other neurodegenerative disorders, spreads through the brain as the disease progresses.
The tau protein helps cause cognitive decline associated with those diseases. The research shows what provokes its accumulation and how it harms nerve cells called neurons. Scientists may be able to leverage these findings to develop new Alzheimer’s treatments that prevent or delay symptom onset, or slow disease progression once symptoms develop.
UVA’s new research also advances efforts to develop blood tests to detect Alzheimer’s at its earliest stages, when it is, in principle, most amenable to treatment. The researchers found that antibodies used in blood tests for measuring this toxic, chemically modified form of tau, called “taupT217,” can easily be fooled into detecting other proteins, which compromises test accuracy. Fortunately, they also showed how this problem can be avoided.
The new research from UVA’s Dr. George Bloom and collaborators is the most comprehensive examination yet of where and how taupT217 accumulates in the brain. The results provide vital insights into the development of Alzheimer’s and possibly other neurological conditions called “non-Alzheimer’s tauopathies.” Those include Parkinson’s disease and chronic traumatic encephalopathy.
“The past few years have witnessed exciting advances in early Alzheimer’s detection by measuring the amount of taupT217 in blood or cerebrospinal fluid, but until now almost nothing has been learned about what causes this type of tau to form in the brain or how it affects neuron health,” said Bloom, of UVA’s Departments of Biology, Cell Biology and Neuroscience, as well as the UVA Brain Institute, the Virginia Alzheimer’s Disease Center and UVA’s Program in Fundamental Neuroscience.
