Neuroinflammation and amyloid deposition in the progression of mixed Alzheimer and vascular dementia

Alzheimer's disease (AD) and vascular contributions to cognitive impairment and dementia (VCID) pathologies commonly coexist in community-dwelling elderly. It is not discernible whether neuroinflammation and amyloid beta (Aβ) deposition are distinct or entangled pathophysiological mechanisms in patients with mixed AD and VCID pathologies. In this study, we found that neuroinflammation (measured by 11C-PK11195 uptake) but not Aβ deposition (measured by 11C-PiB binding), contributes to white matter hyperintensities baseline volume and progression. Both neuroinflammation and Aβ deposition independently contribute to cognitive impairment progression. Neuroinflammation and Aβ deposition represent two distinct pathophysiological pathways in elderly participants with mixed AD and VCID pathologies.