Whenever 27-year-old Nathan Kerr stops by the office of his 81-year-old mentor Frank Booth, Kerr often finds Booth running on a treadmill.

“You’re not going to find someone with more enthusiasm for what they do than Frank,” said Kerr, a postdoctoral fellow at the University of Missouri. “Frank is the definition of someone who practices what they preach — and he has been on a mission to encourage active lifestyles his whole career.”

A comprehensive study of brain scans from more than 600 people sheds new light on the relationship between tau protein and amyloid-β, two central players in the progression of Alzheimer’s disease. The findings provide crucial insight into the disorder’s origins and could inform future strategies to target these proteins for therapeutic purposes. Alzheimer’s disease is intimately linked to aggregates of amyloid-β and tau, which damage neurons and lead to cognitive decline. However, the exact relationship between these two actors is still largely unclear, which has slowed the translation of therapies aimed at halting their accumulation. One of the most popular models of Alzheimer’s disease is the “amyloid cascade model,” which proposes that amyloid-β plaques form first and then trigger the spread of tau proteins. In this study, Sebastian Roemer-Cassiano and colleagues examined a slew of brain imaging data from 140 patients and 69 healthy individuals enrolled in the Alzheimer’s Disease Neuroimaging Initiative. They analyzed functional MRI data and PET scans on tau, glucose metabolism and amyloid-β spread gathered from the patients, discovering that brain regions affected by amyloid-β pathology exhibited higher neuronal activity and connectivity. Specifically, amyloid-β encouraged connections between “epicenters” of tau in the temporal lobe and other regions farther back in the brain, which tend to be more vulnerable to tau aggregates. The scientists replicated their findings in a second group of 345 people with preclinical Alzheimer’s disease and 55 healthy people. “Together, our results should encourage others to further investigate neuronal activity and connectivity as key links between [amyloid-β] and tau to help specifically target the [amyloid-β]-tau axis in Alzheimer’s disease,” the team concludes. For reporters interested in trends, a July 2023 study in Science Translational Medicine involving more than 10,000 middle-aged adults identified 15 proteins linked to a higher risk of dementia and Alzheimer’s disease up to 25 years later: https://www.science.org/doi/10.1126/scitranslmed.adf5681

Researchers from the University of Turku and Åbo Akademi University in Finland and the University of Wisconsin in the United States demonstrated that individuals who had childhood epilepsy have an increased accumulation of brain amyloid later in life, potentially predisposing them to late-onset brain amyloid disorders, such as Alzheimer's disease.

The Davos Alzheimer’s Collaborative (DAC), a pioneering worldwide initiative seeking to advance brain health and resilience throughout life, today announced that Dr. Tedros Adhanom Ghebreyesus, Director-General of the World Health Organization (WHO), will deliver a keynote speech at the DAC Brain House on Tuesday, January 21, at 2:30 p.m. CET, at the World Economic Forum Annual Meeting (WEF) in Davos, Switzerland. Dr. Tedros’ remarks will focus on the importance of adopting a life-course approach to brain health – from youth through middle age and later stages of life. He also will address the challenges and opportunities of conditions such as autism, mental health and dementia.