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Behavior and amyloid profiles modify the association of tauopathy/neurodegeneration and cognitive decline in Alzheimer’s disease
Author(s) -
Ge Xinting,
Qiao Yuchuan,
Zhang Jiong,
Shi Yonggang
Publication year - 2020
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1002/alz.040049
Subject(s) - tauopathy , cognitive decline , neurodegeneration , entorhinal cortex , dementia , psychology , pittsburgh compound b , neuroscience , cognition , alzheimer's disease , neuroimaging , temporal lobe , hippocampus , medicine , disease , cognitive impairment , epilepsy
Background Tau tangles and amyloid plaques are specific biomarkers that define dementia of Alzheimer’s disease (AD). However, behavioral changes or neuropsychiatric symptoms (NPS) are the natural course of AD, which impact the patients’ quality of life and caregivers’ burdens. Relationship between tau tangles or changes of cortical thickness and ‘noncognitive’ symptoms such as behavioral changes were understudied. Method 497 subjects were selected from Alzheimer’s Disease Neuroimaging Initiative (ADNI) project. Participants underwent tau positron emission tomographic (PET) scanning with 18F AV‐1451, Aβ PET scanning with florbetapir or florbetaben, magnetic resonance imaging, and cognitive and behavioral testing. A 4‐group division approach was proposed using both amyloid (A‐/A+) and behavior (B‐/B+) status: A‐B‐, A‐B+, A+B‐ and A+B+. Multivariable linear regression model was used to delineate the relationship of tauopathy/neurodegeneration and cognitive decline for each group. Result The tau deposition increased significantly from the A‐ group to the A+ group, and the associated regions spread into nearly the whole brain. No correlations of the cortical thickness with cognitive decline were found for both the A‐ and A+ groups. Considering the behavior status, no associations were found for both the A‐B‐ group and the A+B‐ group. The association of cognitive decline with tau deposition was observed in the temporal lobe (entorhinal cortex, para‐hippocampal gyrus, et., al) for the A‐B+ group and spread into nearly the whole cerebrum for the A+B+ group. For cortical thickness, the associations with cognitive decline show similar spreading patterns of tau deposition for the A‐B+ group while nearly no difference of the associated regions for the A+B+ group. Conclusion The association of cognitive decline with tauopathy/neurodegeneration were driven by the subjects with abnormal behavior status (B+ groups), while there were nearly no associations for B‐ groups (A‐ and A+). NPS may have the ability to improve the differentiation sensitivity of Aβ on the severity of tauopathy/neurodegeneration. Several factors such as tau tangles, amyloid plaques, cortical atrophy, and behavior symptoms should be considered together for neuropsychiatric disorder diagnosis.