Abstract #0027

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

Chunwei Ying¹, Peter Kang², Michael M. Binkley², Andria L. Ford^1,2, Yasheng Chen², Jason Hassenstab^2,3, Qing Wang^1,3, Jeremy Strain², John C. Morris³, Jin-Moo Lee^1,2, Tammie L. S. Benzinger^1,3,4, and Hongyu An^1,2

¹Mallinckrodt Institute of Radiology, Washington University School of Medicine, St Louis, MO, United States, ²Department of Neurology, Washington University School of Medicine, St Louis, MO, United States, ³Knight Alzheimer Disease Research Center, Washington University School of Medicine, St Louis, MO, United States, ⁴Department of Neurosurgery, Washington University School of Medicine, St Louis, MO, United States

Synopsis

Keywords: Dementia, DementiaAlzheimer'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.

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