The most widely accepted theory behind Alzheimer’s disease currently involves the build-up of amyloid-beta and tau proteins in the brain. While it is known that these proteins play a role in the disease, the exact mechanism is still not clear. Researchers from McGill University conducted a study that found increased levels of both amyloid-beta and tau proteins in the brain may lead to changed brain activity before the cognitive symptoms of Alzheimer’s disease appear. This sheds new light on how these proteins might impact brain function.
Amyloid-beta and tau proteins are naturally found in the brain, but in Alzheimer’s disease, they start to accumulate, potentially altering brain activity and leading to cognitive decline. The study recruited participants with a family history of Alzheimer’s disease and used PET scans to detect the presence of the proteins in the brain. The researchers also recorded brain activity using magnetoencephalography in the areas where the proteins were present. The study found that individuals with elevated levels of both amyloid-beta and tau proteins exhibited changes in brain activity that preceded cognitive symptoms.
The study concluded that individuals with higher levels of amyloid-beta showed signs of brain hyperactivity, while those with higher levels of both amyloid-beta and tau experienced brain slowing or hypoactivity. Participants with hypoactivity also demonstrated increased attention and memory decline. The connection between the early build-up of amyloid-beta and tau, changes in brain activity, and later cognitive deficits highlights the importance of understanding how these proteins impact the brain before symptoms appear. The researchers plan to follow the participants over nearly 10 years to refine predictions of cognitive decline and Alzheimer’s symptoms based on brain scans and cognitive testing.
Neurologist Clifford Segil expressed some skepticism regarding the study’s findings, questioning how the authors determined that participants would have long-term cognitive declines based on the data. He highlighted the controversy surrounding the belief that brain amyloid and tau levels directly cause cognitive issues. Many clinicians remain unconvinced that the build-up of these proteins is pathological and leads to cognitive decline. Segil emphasized the lack of noticeable changes in cognitive abilities in patients receiving anti-amyloid medications, suggesting that amyloid and tau proteins may not be as toxic as once believed.
Segil called for follow-up cognitive testing to determine if individuals with high levels of brain amyloid or tau indeed have poor cognition. He noted that the use of anti-amyloid medications in the United States has not shown meaningful changes in cognitive status in patients, further casting doubt on the relationship between brain proteins and cognitive decline. The study’s findings provide valuable insights into the early changes in brain activity associated with Alzheimer’s disease and the potential impact of amyloid-beta and tau proteins, but further research is needed to fully understand the complexities of the disease.
