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Differential associations between PET and CSF Alzheimer's disease biomarkers and cognition among cognitively normal older adults
Author(s) -
Oh Hwamee,
Correia Stephen,
Salloway Stephen P.
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.041577
Subject(s) - entorhinal cortex , atrophy , psychology , cognition , alzheimer's disease neuroimaging initiative , neuroscience , neuroimaging , cerebrospinal fluid , alzheimer's disease , hippocampus , pathology , disease , medicine , cognitive impairment
Background The presence of brain β‐amyloid (Aβ) plaques among cognitively normal older adults has been related to steeper cognitive decline and an increased risk of Alzheimer’s disease (AD). The co‐presence of tau pathology in these individuals, however, makes it challenging to link AD pathologies to changes in specific cognitive function and brain structure. In addition, it remains unclear whether AD pathologies in the brain and their increased concentration in the cerebrospinal fluid (CSF) have similar effects on cognition. Method We assessed the relationship between Aβ and tau pathology, gray matter atrophy, and cognition among cognitively normal older adults in the Alzheimer's disease neuroimaging initiative whose brain Aβ deposition and tau‐protein neurofibrillary tangles were detected by 18F‐Florbetapir and 18F‐Flortaucipir, respectively. Within a subset of the sample, CSF measures of amyloid (Aβ 40 and Aβ 42 ) and tau (t‐tau and p‐tau) pathologies were assessed in relation to cognition and cortical thickness. Multiple regression models were applied to assess the relationships between AD pathologies, gray matter atrophy, and cognition using region‐of‐interest and whole‐brain surface‐based approaches. Result Higher entorhinal tau PET counts corresponded to greater gray matter atrophy in the entorhinal cortex and hippocampus and poorer executive function performance, controlling for age, sex, and whole‐brain amyloid load. In the subset of the sample, whole‐brain amyloid load related to poorer memory and executive function performance, controlling for age, sex, and CSF total tau. Age was associated with memory and executive function performance, independent of entorhinal tau PET counts, CSF total tau, and whole‐brain amyloid load. Entorhinal tau PET counts did not correlate with CSF total tau or p‐tau among cognitively normal older adults. Conclusion Amyloid and tau pathology differentially influence cognition and brain structure. A low correlation between tau PET and CSF total tau measures in cognitively normal older adults may warrant further investigation on the source of discordance in these measures.