A subtle change in brain wave activity could predict Alzheimer's disease more than two years before diagnosis, according to a new study.
The signal could prove to be a sensitive biomarker of cognitive decline.
Using a noninvasive imaging technique called magnetoencephalography (MEG), neuroscientists at Brown University in the US and Spain's Complutense University of Madrid and University of La Laguna analyzed the resting brain wave activity of 85 patients diagnosed with mild cognitive impairment.
The team discovered distinct differences in the brain wave patterns of participants who went on to later develop Alzheimer's disease. This group produced beta waves at a lower rate, with weaker power, and with a shorter duration than those who did not progress to Alzheimer's within the same period.
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"We've detected a pattern in electrical signals of brain activity that predicts which patients are most likely to develop the disease within two and a half years," says co-lead author and neuroscientist Stephanie Jones from Brown.
"Being able to noninvasively observe a new early marker of Alzheimer's disease progression in the brain for the first time is a very exciting step."
The patterns are consistent with a critical shift in beta-wave activity that typically occurs around age 60 in healthy patients. From this point on, these bursts of activity tend to decline, but those with Alzheimer's typically show a faster progression.
Recently, MEG imaging studies have linked tiny brain wave changes to learning, memory, and executive function, supporting the use of the technique "as a biomarker of cognitive impairment."
It all depends on how the MEG readings are, well, read. They're often analyzed as averages, but this technique can skip over critical detail, argue the researchers behind the new study. They've instead used a closer analytical technique.
Beta-wave bursts were ultimately shorter in those who went on to develop Alzheimer's. Some evidence suggests that beta-wave bursts throughout the brain are a signature of inhibitory control.
The researchers, therefore, suspect that the ability to modulate beta-wave bursts according to the cognitive task at hand is necessary for optimal function.
The associated cognitive decline they observed in those who went on to develop Alzheimer's "may be directly related to lack of inhibitory cognitive control," the researchers write.
The hunch aligns with a leading hypothesis that suggests Alzheimer's disease in its earliest stages is marked by hyperexcitable neurons.
"Now that we've uncovered beta event features that predict Alzheimer's disease progression, our next step is to study the mechanisms of generation using computational neural modeling tools," says Jones.
"If we can recreate what's going wrong in the brain to generate that signal, then we can work with our collaborators to test therapeutics that might be able to correct the problem."
The study was published in Imaging Neuroscience.