Tau accumulation and atrophy predict amyloid independent cognitive decline in aging
Corrina S. Fonseca, Suzanne L. Baker, Lindsey Dobyns, Mustafa Janabi, William J. Jagust, Theresa M. Harrison- Psychiatry and Mental health
- Cellular and Molecular Neuroscience
- Geriatrics and Gerontology
- Neurology (clinical)
- Developmental Neuroscience
- Health Policy
- Epidemiology
Abstract
INTRODUCTION
Amyloid beta (Aβ) and tau pathology are cross‐sectionally associated with atrophy and cognitive decline in aging and Alzheimer's disease (AD).
METHODS
We investigated relationships between concurrent longitudinal measures of Aβ (Pittsburgh compound B [PiB] positron emission tomography [PET]), tau (flortaucipir [FTP] PET), atrophy (structural magnetic resonance imaging), episodic memory (EM), and non‐memory (NM) in 78 cognitively healthy older adults (OA).
RESULTS
Entorhinal FTP change was correlated with EM decline regardless of Aβ, but meta‐temporal FTP and global PiB change were only associated with EM and NM decline in Aβ+ OA. Voxel‐wise analyses revealed significant associations between temporal lobe FTP change and EM decline in all groups. PiB and FTP change were not associated with structural change, suggesting a functional or microstructural mechanism linking these measures to cognitive decline.
DISCUSSION
Our results show that longitudinal Aβ is linked to cognitive decline only in the presence of elevated Aβ, but longitudinal temporal lobe tau is associated with memory decline regardless of Aβ status.
HIGHLIGHTS
Entorhinal tau change was associated with memory decline in older adults (OA), regardless of amyloid beta (Aβ). Greater meta‐region of interest (ROI) tau change correlated with memory decline in Aβ+ OA. Voxel‐wise temporal tau change correlated with memory decline, regardless of Aβ. Meta‐ROI tau and global amyloid change correlated with non‐memory change in Aβ+ OA. Tau and amyloid accumulation were not associated with structural change in OA.