Early detection could help patients start Alzheimer's treatments when they deliver the greatest value to patients, families and society. 

A study published in Alzheimer’s & Dementia identifies changes in blood β-synuclein levels from the third decade of life, around 21 years before the average age at diagnosis of prodromal Alzheimer’s disease in the cohort studied. Changes in this protein appear several years earlier than changes in other blood biomarkers of the disease, such as pTau217, NfL, and GFAP. Elevated β-synuclein levels are also associated with poorer memory performance and with structural and metabolic changes in brain regions affected by Alzheimer’s disease. In the future, β-synuclein could complement other biomarkers to better characterize and monitor the earliest stages of the disease, select participants for clinical trials, and study responses to treatment.

Understanding the mechanisms that stabilize distinct tau filament structures may help explain why tau-related neurodegenerative diseases develop different pathological features. A researcher now at the University of Tsukuba, together with colleagues at the University of Pennsylvania, analyzed the tau filaments that accumulate in the brains of patients with neurodegenerative diseases such as Alzheimer's disease. They found that, in certain tau filaments, repositioning the polyubiquitin attached to tau changes not only the surrounding molecular environment but also the filament core structure itself. The findings suggest that the spatial arrangement of post-translational modifications around the filament core helps stabilize disease-specific tau filament structures.