Abstract
INTRODUCTION
The spatial and temporal patterns of cortical mean diffusivity (cMD), as well as its association with Alzheimer’s disease (AD) and suspected non-Alzheimer’s pathophysiology (SNAP), are not yet fully understood.
METHODS
We compared baseline (n = 617) and longitudinal changes (n = 421) of cMD, cortical thickness, and gray matter volume and their relations to vascular risk factors, amyloid beta (Aβ), and tau positron emission tomography (PET), and longitudinal cognitive decline in Aβ PET negative and positive older adults.
RESULTS
cMD increases were more sensitive to detecting brain structural alterations than cortical thinning and gray matter atrophy. Tau-related cMD increases partially mediated Aβ-related cognitive decline in AD, whereas vascular disease-related increased cMD levels substantially mediated age-related cognitive decline in SNAP.
DISCUSSION
These findings revealed the dynamic changes of microstructural and macrostructural indicators and their associations with AD and SNAP, providing novel insights into understanding upstream and downstream events of cMD in neurodegenerative disease.
Highlights
Cortical mean diffusivity (cMD) was more sensitive to detecting structural changes than macrostructural factors.
Tau-related cMD increases partially mediated amyloid beta–related cognitive decline in Alzheimer’s disease (AD).
White matter hyperintensity–related higher cMD mainly explained the age-related cognitive decline in suspected non-Alzheimer’s pathophysiology (SNAP).
cMD may assist in tracking earlier neurodegenerative signs in AD and SNAP.
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This post is Copyright: Pan Sun,
Zhengbo He,
Anqi Li,
Jie Yang,
Yalin Zhu,
Yue Cai,
Ting Ma,
Shaohua Ma,
Tengfei Guo,
Alzheimer’s Disease Neuroimaging Initiative | August 12, 2024