Study: Tracking Alzheimer’s in Healthy People Now Possible
There’s a new way of tracking Alzheimer’s in people without any signs of the disease. It could provide the path to diagnosing the disease in healthy people by measuring the degree of protein accumulation in their brains.
Previously, the only way to confirm the disease was through autopsies.
Now, researchers at the University of California, Berkeley, show for the first time that PET scans can track the progressive stages of Alzheimer’s disease in cognitively normal adults.
The findings, published this week in the journal Neuron, come from positron emission tomography (PET) of 53 adults. Five were young adults aged 20-26, 33 were cognitively healthy adults aged 64-90, and 15 were patients aged 53-77 who had been diagnosed with probable Alzheimer’s dementia.
In the process, the scientists also obtained important clues about two Alzheimer’s-linked proteins — tau and beta-amyloid — and how they relate to each other.
“Our study is the first to show the staging in people who are not only alive, but who have no signs of cognitive impairment,” said Dr. William Jagust. “This opens the door to the use of PET scans as a diagnostic and staging tool.”
The research also shed light on the nature of tau and amyloid protein deposits in the aging brain.
For many years, the accumulation of beta amyloid plaques was considered the primary culprit in Alzheimer’s disease. Over the past decade, however, tau, a protein important in maintaining the structure of neurons, has emerged as a major player. When the tau protein gets tangled and twisted, its ability to support synaptic connections becomes impaired.
While a number of symptoms exist that signal Alzheimer’s disease, a definitive diagnosis has been possible only through an examination of the brain after the patient has died. The availability of amyloid imaging for the past decade has improved this situation, but how Alzheimer’s developed as a result of amyloid remains a mystery.
Studies done in autopsies linked the development of symptoms to the deposition of the tau protein.
Through the PET scans, the researchers confirmed that with advancing age, tau protein accumulated in the medial temporal lobe — home to the hippocampus and the memory centre of the brain.
“Tau is basically present in almost every aging brain,” said study co-author Michael Schöll. “Very few old people have no tau. In our case, it seems like the accumulation of tau in the medial temporal lobe was independent of amyloid and driven by age.”
The study revealed that higher levels of tau in the medial temporal lobe were associated with greater declines in episodic memory, the type of memory used to code new information. The researchers tested episodic memory by asking subjects to recall a list of words viewed 20 minutes earlier.
One question yet to be answered is why so many people who have tau in their medial temporal lobe never go on to develop Alzheimer’s. Likewise, adults may have beta amyloid in their brains and still be cognitively healthy.
“It’s not that one is more important than the other,” said researcher Samuel Lockhart. ”Our study suggests that they may work together in the progression of Alzheimer’s.”
“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,” said Jagust. “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.”