Automated method monitors cortical origin and initial release of TAU proteins in Alzheimer’s disease

Researchers have developed an automated method that will be able to monitor the development of harmful clusters of TAU proteins associated with Alzheimer’s disease in the brain, according to work involving 443 individuals. The method revealed that TAU ​​first appeared in an area of ​​the brain called the rhinal cortex before spreading elsewhere, suggesting that targeting TAU here may delay the progression of Alzheimer’s disease.

The uptake of toxic proteins amyloid-beta and TAU is responsible for many of the symptoms and damage to neurons seen in Alzheimer’s disease. However, conventional therapies have shown less efficacy, at least in part because the therapies were administered long after the protein had spread throughout the brain. The development of more effective interventions therefore requires a better understanding of where TAU pathology originated and how it spreads. Justin Sanchez and his colleagues designed an automated anatomic sampling method that uses PET imaging to monitor the presence of TAU in the brain.

The team applied their strategy to 443 participating adults – including 55 patients with Alzheimer’s – and found that TAU ​​deposits in the rhinal cortex appeared independently from amyloid-beta before they spread to the temporal neocortex. A two-year trial with 104 subjects showed that people with the highest initial levels of TAU or beta amyloid exhibited the greatest distribution of TAU throughout the brain by the end of the study.

“Those decisions suggest that [the rhinal cortex] is a biomarker of downstream TAU deployment … with potential convenience for therapeutic experiments in which TAU diffusion is a measure of yield, ”the authors conclude.