Amyloid-β and Tau Cause Measurable Loss of Brain Function Prior to Evident Symptoms of Alzheimer's
Evidence suggests that Alzheimer's disease develops slowly over time for potentially decades prior to the emergence of symptoms. Researchers here made use of healthy patients with a familial history of Alzheimer's to assess the early stages of the development of the condition. The researchers measured the presence of protein aggregates and their interaction, as well as markers of brain activity. Their results show that even absent evident Alzheimer's disease, a greater presence of protein aggregates correlates with loss of cognitive function.
Amyloid-beta and tau proteins have long been associated with Alzheimer's disease. Researchers recruited 104 people with a family history of Alzheimer's. They scanned the participants' brains using a combination of positron emission tomography (PET) to detect the presence and location of the proteins and magnetoencephalography (MEG) to record brain activity in these regions. The scientists compared the results of the two scans and found that brain areas with increased levels of amyloid-beta showed macroscopic expressions of brain hyperactivity, reflected by increased fast- and decreased slow-frequency brain activity. For people with both amyloid-beta and tau in their brain, the pattern shifted towards hypoactivity, with higher levels of pathology leading to brain activity slowing.
Using cognitive tests, the team discovered that participants with higher rates of this amyloid-tau related brain slowing showed higher levels of decline in attention and memory. The findings suggest that the interplay between amyloid-beta and tau lead to altered brain activity before noticeable cognitive symptoms appear. In a follow up study, researchers plans to rescan the same participants over time to prove whether the accumulation of the two proteins promotes further slowing of brain activity, and whether this accurately predicts the cognitive evolution of the participants.