Authors: Alice Weatherston
Scientists at the University of California Berkeley (CA, USA) have recently shown for the first time that positron emission tomography (PET) scans are capable of tracking the progression of Alzheimer’s disease in cognitively ‘normal’ adults. The findings, which were published in Neuron, may provide an important advancement for early diagnosis and management of the disease.
The study included 53 adults separated into three different groups; five were healthy 20–26 year olds, 33 were cognitively healthy 64–90 year olds and 15 were aged 53–77 and had been diagnosed with probable Alzheimer’s dementia.
Braak staging of tau deposition has been established for some time, but was previously only identifiable through postmortem analyses. William Jagust’s (principal investigator; UC Berkeley) new study indicated that PET scans are capable of identifying the neuropathological stages of tau deposition comparably to brain section analysis. “Our study is the first to show the staging in people who are not only alive, but who have no signs of cognitive impairment. This opens the door to the use of PET scans as a diagnostic and staging tool.” explained Jagust.
The PET scans also revealed new information about the role of tau and beta-amyloid in Alzheimer’s development and their associated roles.
With increase in age, tau proteins were shown to accumulate in the medial temporal lobe, regardless of cognitive health. “Tau is basically present in almost every aging brain. 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,” commented co-lead author Michael Schöll (UC Berkeley).
On the role of tau and beta-amyloid, Samuel Lockhart (another co-lead author on the study, UC Berekley) commented: “It’s not that one is more important than the other. Our study suggests that they may work together in the progression of Alzheimer’s.”
While increased levels of tau within the medial temporal lobe were associated with declines in episodic memory, the PET scans revealed that it was the spread of tau to other regions of the brain that lead to more serious, Alzheimer’s-like declines in cognitive function. Importantly this spread was also linked with the presence of amyloid plaques.
“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,” remarked 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.”
The team believe that the study helps to highlight the use of PET scans for tau imaging, which may become an important method in helping to develop therapeutic approaches for targeting either tau or amyloid at relevant disease stages.