Dr. William Jagust explains how tau and beta amyloid, two proteins associated with Alzheimer’s disease, develop in the aging brain, which his research team has visualized using positron emission tomography, or PET, scans. Photo by Stephen McNally/University of California Berkeley
BERKELEY, Calif., March 3 (UPI) -- Researchers have visualized the development of Alzheimer's disease in the brain in living people using positron emission tomography, or PET scans, which they say will aid with its diagnosis and treatment.
Tau and beta-amyloid build-ups in the brain were seen in scans of healthy people and patients diagnosed with Alzheimer's, showing the disease's development and offering clues about how it progresses.
Alzheimer's disease is typically diagnosed using several cognitive indicators, but there has been no way to verify the diagnosis until a patient dies, when Braak staging is used to determine tau deposition during an autopsy.
The researchers found they could see build-ups of both substances in the brain, which disrupt synaptic connections, and the formation of new memories and recall of old ones. Recent studies have shown the brain shows signs of the disease earlier in life, seeing build-ups in the brain as they happen could help doctors prevent or delay onset of the disease.
"Braak staging was developed through data obtained from autopsies, but our study is the first to show the staging in people who are not only alive, but who have no signs of cognitive impairment," Dr. William Jagust, a professor at the University of California Berkeley's School of Public Health, in a press release. "This opens the door to the use of PET scans as a diagnostic and staging tool."
For the study, published in the journal Neuron, researchers recruited five young adults between the age of 20 and 26, 33 cognitively healthy adults between age 64 and 90, and 15 Alzheimer's patients between age 53 and 77.
The researchers found they were able to rank the tau and beta amyloid build-ups accurately with the cognitive abilities and diagnoses of the participants.
Shown are PET scans that track tau, the top row, and beta-amyloid from two normal older people and one patient with Alzheimer’s disease. The normal older adult on the left has no brain amyloid deposition and minimal tau in the medial temporal lobe. In the normal older adult in the middle, amyloid deposition is present throughout the brain, and tau has spread out into the temporal cortex. In the Alzheimer's disease patient, both amyloid and tau are spread through the brain. Photo by Michael Schöll/University of California Berkeley
With the scans, the researchers confirmed tau protein accumulation in the medial temporal lobe, where the hippocampus and memory center of the brain are located, is present in nearly all aging brains.
While the researchers are unsure why many people with build-ups of tau do not go on to develop the disease, higher levels disrupt brain function in the disease, and appear to interact somehow with the formation of amyloid -- and work together in the progression of Alzheimer's disease.
"Amyloid may somehow facilitate the spread of tau, or tau may initiate the deposition of amyloid. We don't know. We can't answer that at this point," Jagust said. "All I can say is that when amyloid starts to show up, we start to see tau in other parts of the brain, and that is when real problems begin. We think that may be the beginning of symptomatic Alzheimer's disease."