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. While amyloid-beta starts accumulating early in the aging brain, it alone isn’t enough to cause Alzheimer’s. The accumulation of tau comes later, and together, these proteins are present in the brains of Alzheimer’s patients. However, how the earliest deposits affect brain activity in humans, especially before cognitive symptoms appear, wasn’t well understood. The study used positron emission tomography (PET) and magnetoencephalography (MEG) to look for signs of the two proteins in the brain as well as record brain activity in the affected areas.
It was found that individuals with increased levels of amyloid-beta showed signs of brain hyperactivity, while those with higher levels of both amyloid-beta and tau proteins experienced hypoactivity or brain slowing. Participants with hypoactivity also had increased levels of attention and memory decline. This early slowing of brain activity in the presence of both proteins was found to be predictive of later cognitive decline three to four years after the brain scans were collected. The study highlighted the importance of understanding the impact of amyloid-beta and tau proteins on the brain and how brain activity may alter before symptoms appear. Further research involving the same participants over nearly 10 years with follow-up imaging and cognitive testing is ongoing to refine predictions of cognitive decline and Alzheimer’s symptoms.
Neurologist Clifford Segil from Providence Saint John’s Health Center in California expressed confusion about the study’s conclusions, questioning the link between the participants’ amyloid and tau levels and long-term cognitive declines. He mentioned that many clinical neurologists remain unconvinced that the build-up of these proteins in the brain leads to cognitive decline. He noted that the clinical use of anti-amyloid medications has not shown meaningful changes in cognitive abilities, leading to skepticism about the role of amyloid and tau proteins in causing memory loss. Segil emphasized the need for follow-up cognitive testing to determine if there is a direct relationship between high levels of brain amyloid or tau and poor cognition.
The study conducted by McGill University sheds light on the impact of amyloid-beta and tau proteins on brain activity before the onset of cognitive symptoms in Alzheimer’s disease. The research found that increased levels of both proteins may lead to altered brain activity, with individuals experiencing hypoactivity and memory decline. The study’s findings provide valuable insights into the role of these proteins in the development of Alzheimer’s disease and the potential predictive value of changes in brain activity for later cognitive decline. Further research involving long-term follow-up of participants is ongoing to refine predictions of cognitive decline and Alzheimer’s symptoms.
The study involved the use of PET and MEG imaging to identify amyloid-beta and tau proteins in the brain and record brain activity in affected areas. The results indicated a clear association between increased levels of both proteins and changes in brain activity, highlighting the importance of understanding the early impact of amyloid-beta and tau on brain function. The findings suggest that altered brain activity in the presence of these proteins may be an early indicator of later cognitive decline in individuals at risk of developing Alzheimer’s disease. Continued research involving the same participants over a decade will provide further insights into the predictive value of brain activity changes for cognitive outcomes.
Neurologist Clifford Segil expressed skepticism about the study’s conclusions, emphasizing the need for further research to validate the link between amyloid and tau proteins and cognitive decline. He noted that clinical observations of patients receiving anti-amyloid medications have not shown significant improvements in cognitive abilities, suggesting that the role of these proteins in causing memory loss may be less significant than previously thought. Segil called for additional cognitive testing to assess the relationship between high levels of brain amyloid or tau and cognitive function, highlighting the ongoing debate among clinicians regarding the pathological implications of these proteins in Alzheimer’s disease.
