PET scans can apparently track Alzheimer’s progression in the brain – aiding early diagnosis and providing new insight into 2 different proteins associated with the disease
Previous knowledge of the timeline of Alzheimer’s disease has largely been established from autopsies and post-mortem analysis, and this data led to the Braak staging method. This method classifies different stages of the condition according to autopsy data. While the method has been extremely helpful, now using a particular scanning method in living patients could reveal in greater detail exactly what’s going on inside a brain diagnosed with Alzheimer’s dementia.
“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”
Tracing the disease timeline
Research at UC Berkeley used positron emission topography (PET) to scan the brains of 53 adults. 5 of these were aged 20-26, 33 healthy adults between 64-90 and 15 between 53-77 who had been recently diagnosed with Alzheimer’s. Their scans confirmed similar stages as presented in the Braak system, which in itself could help identify at risk patients and boost early diagnosis rates.
A question of tau or amyloid
There are two primary culprits in Alzheimer’s called tau and beta-amyloid. Amyloid forms plaques that surround neurons and was believed for a long time to be the cause of the disease, but another protein called tau has gained support in recent years. Tau stabilises microtubules inside neurons, which are effectively cellular scaffolding reinforcing structures and enabling synaptic communication. Both appear to accumulate and malfunction in Alzheimer’s, but we don’t really know exactly what’s going on yet, or who’s really to blame (if either are).
These new scans actually deciphered that tau accumulates in the medial temporal lobe as we get older, a region containing the hippocampus and involved with memory and neurogenesis. The research also discovered that higher levels of tau were associated with poorer memory performance in test subjects.
“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”
Both could be key
Curiously, many people with either tau or amyloid present individually don’t develop dementia symptoms. What these scans discovered that was really interesting however, is that when tau spreads beyond the medial temporal lobe cognitive function begins to decline. This spread coincides with amyloid plaque build up within the brain – leading the scientists to suggest that both are required for disease onset.
“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. 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”
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