MRI Scans Might Reveal Signs of Alzheimer’s Disease Seven Years Before a Telltale Marker Appears in the Brain
Not all researchers are convinced that the brain changes detected via MRI are robust enough to become a diagnostic tool. But the findings could help researchers better understand the mechanisms that drive the neurodegenerative disease
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Alzheimer’s disease is a devastating neurodegenerative disorder and the most common form of dementia. It’s marked by the abnormal buildup of two proteins in the brain—tangles of tau and sticky plaques of beta-amyloid—that damage nerve cells.
Physicians can currently use PET scans to search for amyloid plaques. People already experiencing cognitive decline tend to seek them out to determine whether they have Alzheimer’s.
Now, researchers say a different kind of brain imaging can help them see signs associated with the disease even sooner. Changes in the thickness of the cortex—the brain’s wrinkly outer layer—viewed via MRI scans seem to precede abnormal amyloid buildup and can be detected at least seven years before the protein is detected in PET scans. The findings, published in the journal Nature Neuroscience on August 19, could help researchers better understand the beginnings of Alzheimer’s, which affects more than seven million Americans ages 65 and older.
“We found that structural changes in the brain occur many years before high levels of plaque are seen on PET scans, which is the brain scan currently used to identify the earliest signs of Alzheimer’s disease,” says study co-author James Michael Roe, a neuroscientist at the University of Oslo in Norway, in a statement.
Roe and colleagues examined longitudinal data from more than 1,000 adults who did not have dementia when they enrolled in the research. Participants were followed for up to 16 years and had multiple MRI scans throughout that time. Nearly 700 of them also had amyloid-PET scans. Together, the data allowed the researchers to look at differences in the brains of people who developed Alzheimer’s and those who didn’t, as well as compare what appeared in the two imaging techniques—and when.
Analyses revealed an association between cortical thickness and people who developed amyloid plaques years later. The wrinkly layer naturally thins with age, but it remained a bit thicker in people who eventually showed elevated amounts of beta-amyloid than those who did not. The changes seen via MRI were visible at least seven years before plaques could be viewed via PET scan.
The findings suggest a potential for earlier interventions, says Lucy Hooper, a physician and co-founder of Coyne Medical, a London-based private clinic, who was not involved in the study, to Maria Azzurra Volpe at Newsweek. “Showing that Alzheimer’s develops over years means that the window to prevent or delay the disease is longer.”
Hooper also points out that other markers, like changes in cerebrospinal fluid and blood, can be detected before amyloid buildup in PET scans, further suggesting that Alzheimer’s begins long before it’s identified by conventional imaging.
However, the changes in cortical thickness are probably too subtle to use to diagnose the neurodegenerative disease, says Frederik Barkhof, a neuroradiologist at University College London who also wasn’t involved in the work, to Skyler Ware at Science News. Still, he thinks the results can help researchers understand the drivers of Alzheimer’s disease and emerging treatments.
Did you know? An experimental Alzheimer’s drug targeting tau
Amyloid plaques have been a major target for Alzheimer’s drugs. That’s the course of action of two therapies that were recently approved by the Food and Drug Administration—the first new ones for the disease in about two decades. However, clinical trial data presented in July suggests that an experimental anti-tau drug can slow cognitive decline in people with early-stage Alzheimer’s at a level on par with the greenlit anti-amyloid medicines.
Study co-author Anders Martin Fjell, a neuroscientist at the University of Oslo, echoes that sentiment, noting that the findings hint that there are brain changes in Alzheimer’s that come long before the first detectable signs of beta-amyloid buildup. That could mean either that processes driving plaque accumulation happen before these clumps are visible via PET scans or that other processes in the brain start before beta-amyloid begins to cluster.
“If the latter is true, it suggests it is important to continue developing drugs that target processes other than amyloid plaque accumulation,” Fjell says in the statement. “But we need more research on this.”
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