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Alzheimer Disease-associated Cortical Atrophy Does not Differ Between Chinese and Whites.

ABSTRACT: PURPOSE:To assess whether there are differences in Alzheimer disease (AD)-associated atrophy regions in Chinese and white patients with AD versus cognitively normal older adults, and to test whether associations between clinical severity and gray matter volume are similar or different across these ethnic groups in a cross-sectional analysis. MATERIALS AND METHODS:Chinese and white patients with AD, individuals with mild cognitive impairment, and cognitively normal controls (46 white and 48 Chinese) were clinically evaluated at an academic center within 1 year of magnetic resonance imaging acquisition. Clinical severity was assessed using the Clinical Dementia Rating Sum of Boxes and cortical atrophy was measured using voxel-based morphometry as well as Freesurfer. Chinese and white cohorts were demographically matched for age, sex, and education. RESULTS:Clinical severity by diagnosis was similar across ethnicities. Chinese and white patient groups showed similar amounts of atrophy in the regions most affected in AD after accounting for demographic variables and head size. There was no significant difference between ethnic groups when compared by atrophy and clinical severity. CONCLUSIONS:Our study suggests that Chinese and white patients with AD, when matched demographically, are clinically and neuroanatomically similar on normalized measures of cortical atrophy and clinical severity.

SUBMITTER: Fan J

PROVIDER: S-EPMC6527333 | biostudies-literature | 2019 Jul-Sep

REPOSITORIES: biostudies-literature

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Alzheimer Disease-associated Cortical Atrophy Does not Differ Between Chinese and Whites.

Fan Jia J Tse Marian M Carr Jessie S JS Miller Bruce L BL Kramer Joel H JH Rosen Howard J HJ Bonham Luke W LW Yokoyama Jennifer S JS

Alzheimer disease and associated disorders 20190701 3

<h4>Purpose</h4>To assess whether there are differences in Alzheimer disease (AD)-associated atrophy regions in Chinese and white patients with AD versus cognitively normal older adults, and to test whether associations between clinical severity and gray matter volume are similar or different across these ethnic groups in a cross-sectional analysis.<h4>Materials and methods</h4>Chinese and white patients with AD, individuals with mild cognitive impairment, and cognitively normal controls (46 whi ...[more]

PMID: 31094707

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Project description:Defining a signature of cortical regions of interest preferentially affected by Alzheimer disease (AD) pathology may offer improved sensitivity to early AD compared to hippocampal volume or mesial temporal lobe alone. Since late-onset Alzheimer disease (LOAD) participants tend to have age-related comorbidities, the younger-onset age in autosomal dominant AD (ADAD) may provide a more idealized model of cortical thinning in AD. To test this, the goals of this study were to compare the degree of overlap between the ADAD and LOAD cortical thinning maps and to evaluate the ability of the ADAD cortical signature regions to predict early pathological changes in cognitively normal individuals. We defined and analyzed the LOAD cortical maps of cortical thickness in 588 participants from the Knight Alzheimer Disease Research Center (Knight ADRC) and the ADAD cortical maps in 269 participants from the Dominantly Inherited Alzheimer Network (DIAN) observational study. Both cohorts were divided into three groups: cognitively normal controls (nADRC = 381; nDIAN = 145), preclinical (nADRC = 153; nDIAN = 76), and cognitively impaired (nADRC = 54; nDIAN = 48). Both cohorts underwent clinical assessments, 3T MRI, and amyloid PET imaging with either 11C-Pittsburgh compound B or 18F-florbetapir. To generate cortical signature maps of cortical thickness, we performed a vertex-wise analysis between the cognitively normal controls and impaired groups within each cohort using six increasingly conservative statistical thresholds to determine significance. The optimal cortical map among the six statistical thresholds was determined from a receiver operating characteristic analysis testing the performance of each map in discriminating between the cognitively normal controls and preclinical groups. We then performed within-cohort and cross-cohort (e.g. ADAD maps evaluated in the Knight ADRC cohort) analyses to examine the sensitivity of the optimal cortical signature maps to the amyloid levels using only the cognitively normal individuals (cognitively normal controls and preclinical groups) in comparison to hippocampal volume. We found the optimal cortical signature maps were sensitive to early increases in amyloid for the asymptomatic individuals within their respective cohorts and were significant beyond the inclusion of hippocampus volume, but the cortical signature maps performed poorly when analyzing across cohorts. These results suggest the cortical signature maps are a useful MRI biomarker of early AD-related neurodegeneration in preclinical individuals and the pattern of decline differs between LOAD and ADAD.

Project description:ObjectiveTo examine the cross-sectional associations between regional tau, β-amyloid (Aβ), and cortical thickness and neuropsychological function across the preclinical and clinical spectrum of Alzheimer disease (AD).MethodsWe included 106 participants from the Swedish Biomarkers for Identifying Neurodegenerative Disorders Early and Reliably (BioFINDER) study, of whom 33 had preclinical AD (Aβ-positive cognitively normal individuals), 25 had prodromal AD (Aβ-positive mild cognitive impairment), and 48 had probable AD dementia. All underwent [18F]flortaucipir (tau) and structural MRI (cortical thickness), and 88 of 106 underwent [18F]flutemetamol (Aβ) PET. Linear regression models adjusted for age, sex, and education were performed to examine associations between 7 regions of interest and 7 neuropsychological tests for all 3 imaging modalities.ResultsIn preclinical AD, [18F]flortaucipir, but not [18F]flutemetamol or cortical thickness, was associated with decreased global cognition, memory, and processing speed (range standardized β = 0.35-0.52, p < 0.05 uncorrected for multiple comparisons). In the combined prodromal AD and AD dementia group, both increased [18F]flortaucipir uptake and reduced cortical thickness were associated with worse performance on a variety of neuropsychological tests (most regions of interest survived correction for multiple comparisons at p < 0.05), while increased [18F]flutemetamol uptake was specifically associated with lower scores on a delayed recall memory task (p < 0.05 uncorrected for multiple comparisons). The strongest effects for both [18F]flortaucipir and cortical thickness on cognition were found in the lateral and medial parietal cortex and lateral temporal cortex. The effect of [18F]flutemetamol on cognition was generally weaker and less region specific.ConclusionOur findings suggest that tau PET is more sensitive than Aβ PET and measures of cortical thickness for detecting early cognitive changes in preclinical AD. Furthermore, both [18F]flortaucipir PET and cortical thickness show strong cognitive correlates at the clinical stages of AD.

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Alzheimer Disease-associated Cortical Atrophy Does not Differ Between Chinese and Whites.

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Alzheimer Disease-associated Cortical Atrophy Does not Differ Between Chinese and Whites.

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