The cause of Alzheimer’s disease is still largely unknown, but the most widely accepted theory involves the build-up of amyloid-beta and tau proteins in the brain. While the role of these proteins in Alzheimer’s has been well-established, researchers are still unclear as to how they might actually cause the disease. A recent study from McGill University found that people with increased levels of both amyloid-beta and tau proteins in the brain may experience altered brain activity before the cognitive symptoms of Alzheimer’s disease appear. This sheds new light on the relationship between these proteins and the onset of the disease.
Amyloid-beta is a sticky protein that forms plaques between brain cells, blocking communication and causing inflammation, while tau proteins tangle inside cells, disrupting function and leading to cell death. The study found that individuals with higher levels of both amyloid-beta and tau proteins experienced hypoactivity or brain slowing, as opposed to those with just amyloid-beta who showed signs of brain hyperactivity. This early slowing of brain activity was found to be predictive of later cognitive decline, highlighting the importance of understanding the impact of these proteins on the brain before symptoms appear.
The study recruited 104 participants with a family history of Alzheimer’s disease and used PET scans to detect amyloid-beta and tau proteins, as well as MEG scans to record brain activity in these areas. The findings suggest that the combination of amyloid-beta and tau proteins leads to changes in brain activity that may contribute to the development of Alzheimer’s disease. The next steps for researchers involve ongoing follow-up studies with the same participants over nearly 10 years to refine their ability to predict cognitive decline and Alzheimer’s symptoms from brain scans.
While the study provides valuable insights into the relationship between amyloid-beta, tau proteins, and changes in brain activity, some experts remain skeptical about the role of these proteins in causing cognitive decline. Neurologist Clifford Segil points out that the clinical use of anti-amyloid medications in practice has not shown significant changes in cognitive abilities, leading some to question the link between amyloid and tau proteins and dementia symptoms. Further research is needed to determine the true impact of these proteins on cognitive function and the development of Alzheimer’s disease.
The findings from the McGill University study have the potential to inform future research and clinical practice in the diagnosis and treatment of Alzheimer’s disease. Understanding how amyloid-beta and tau proteins influence brain activity and cognitive decline before symptoms appear could lead to earlier detection and intervention strategies. By continuing to follow the study participants over time and refining predictive models, researchers hope to improve their ability to identify individuals at risk for Alzheimer’s and develop more effective treatment approaches. The data collected from these studies will be made available to other researchers for replication and further exploration of these important findings.
