This study changes our view of Alzheimer’s disease (AD) initiation and progression. Mutations promoting cerebral beta-amyloid (Aβ) deposition guarantee rare genetic forms of AD. Thus, the prevailing hypothesis has been that Aβ is central to initiation and progression of all AD, despite contrary animal and patient evidence. We show that age-related T cells generate neurodegeneration with compelling features of AD in mice, with distinct T cell functions required for pathological initiation and neurodegenerative progression. Knowledge from these mice was applied to successfully predict previously unrecognized features of human AD and generate tools for its clinical management.

Read full publication at https://www.pnas.org/doi/10.1073/pnas.2401420121