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1.  Ventricular atrophy and its clinical correlates in the imaging cohort from the ADCS MCI Donepezil/Vitamin E study 
We analyzed the baseline and 3-year T1-weighted magnetic resonance imaging data of 110 amnestic mild cognitive impairment (MCI) participants with minimal hippocampal atrophy at baseline from the Alzheimer’s Disease Cooperative Study group (ADCS) MCI Donepezil/Vitamin E trial. 46 subjects converted to AD (MCIc) while 64 remained stable (MCInc). We used the radial distance technique to examine the differences in lateral ventricle shape and size between MCIc and MCInc and the associations between ventricular enlargement and cognitive decline.
MCIc group had significantly larger frontal and right body/occipital horns relative to MCInc at baseline and significantly larger bilateral frontal, body/occipital and left temporal horns at follow-up. Global cognitive decline measured with ADAScog and MMSE and decline in activities of daily living (ADL) were associated with posterior lateral ventricle enlargement. Decline in ADAScog and ADL were associated with left temporal and decline in MMSE with right temporal horn enlargement. After correction for baseline hippocampal volume decline in ADL showed a significant association with right frontal horn enlargement. Executive decline was associated with right frontal and left temporal horn enlargement.
PMCID: PMC3662002  PMID: 23694947
Alzheimer’s disease; AD; mild cognitive impairment; MCI; imaging; MRI; brain atrophy; ventricular enlargement
2.  Vascular and Alzheimer's disease markers independently predict brain atrophy rate in Alzheimer's Disease Neuroimaging Initiative controls 
Neurobiology of Aging  2013;34(8):1996-2002.
This study assessed relationships among white matter hyperintensities (WMH), cerebrospinal fluid (CSF), Alzheimer's disease (AD) pathology markers, and brain volume loss. Subjects included 197 controls, 331 individuals with mild cognitive impairment (MCI), and 146 individuals with AD with serial volumetric 1.5-T MRI. CSF Aβ1-42 (n = 351) and tau (n = 346) were measured. Brain volume change was quantified using the boundary shift integral (BSI). We assessed the association between baseline WMH volume and annualized BSI, adjusting for intracranial volume. We also performed multiple regression analyses in the CSF subset, assessing the relationships of WMH and Aβ1-42 and/or tau with BSI. WMH burden was positively associated with BSI in controls (p = 0.02) but not MCI or AD. In multivariable models, WMH (p = 0.003) and Aβ1-42 (p = 0.001) were independently associated with BSI in controls; in MCI Aβ1-42 (p < 0.001) and tau (p = 0.04) were associated with BSI. There was no evidence of independent effects of WMH or CSF measures on BSI in AD. These data support findings that vascular damage is associated with increased brain atrophy in the context of AD pathology in pre-dementia stages.
PMCID: PMC3810644  PMID: 23522844
Alzheimer's disease; Vascular disease; Mild cognitive impairment (MCI); Volumetric MRI; Normal aging
3.  Mediterranean Diet and Magnetic Resonance Imaging–Assessed Cerebrovascular Disease 
Annals of neurology  2011;69(2):257-268.
Cerebrovascular disease is 1 of the possible mechanisms of the previously reported relationship between Mediterranean-type diet (MeDi) and Alzheimer’s disease (AD). We sought to investigate the association between MeDi and MRI infarcts.
High-resolution structural MRI was collected on 707 elderly 65 years or older community residents of New York with available dietary assessments administered an average of 5.8 years (3.22 standard deviations [SDs]) before the MRI. Participants were divided into 3 groups of adherence to MeDi (low, middle, and high tertiles). We examined the association of increasing adherence to MeDi with presence of infarcts on MRI. Models were run without adjustment, adjusted for basic demographic and clinical factors, and adjusted for vascular risk factors.
A total of 222 participants had at least 1 infarct. In the unadjusted model, compared to the low adherence group, those in the moderate MeDi adherence group had a 22% reduced odds of having an infarct (odds ratio [OR], 0.78; 95% confidence interval [CI], 0.55–1.14), while participants in the highest MeDi adherence group had a 36% reduced odds (OR, 0.64; 95% CI, 0.42–0.97; p for trend = 0.04). In adjusted models, the association between MeDi adherence and MRI infarcts remained essentially unchanged. The association of high MeDi adherence with infarcts was comparable to that of hypertension (40% reduced probability), did not vary by infarct size or after excluding patients with dementia (n = 46) or clinical strokes (n = 86). There was no association between MeDi and white matter hyperintensities.
Higher adherence to the MeDi is associated with reduced cerebrovascular disease burden.
PMCID: PMC3066080  PMID: 21387371
4.  Cognitive reserve and Alzheimer's disease biomarkers are independent determinants of cognition 
Brain  2011;134(5):1479-1492.
The objective of this study was to investigate how a measure of educational and occupational attainment, a component of cognitive reserve, modifies the relationship between biomarkers of pathology and cognition in Alzheimer's disease. The biomarkers evaluated quantified neurodegeneration via atrophy on magnetic resonance images, neuronal injury via cerebral spinal fluid t-tau, brain amyloid-β load via cerebral spinal fluid amyloid-β1–42 and vascular disease via white matter hyperintensities on T2/proton density magnetic resonance images. We included 109 cognitively normal subjects, 192 amnestic patients with mild cognitive impairment and 98 patients with Alzheimer's disease, from the Alzheimer's Disease Neuroimaging Initiative study, who had undergone baseline lumbar puncture and magnetic resonance imaging. We combined patients with mild cognitive impairment and Alzheimer's disease in a group labelled ‘cognitively impaired’ subjects. Structural Abnormality Index scores, which reflect the degree of Alzheimer's disease-like anatomic features on magnetic resonance images, were computed for each subject. We assessed Alzheimer's Disease Assessment Scale (cognitive behaviour section) and mini-mental state examination scores as measures of general cognition and Auditory–Verbal Learning Test delayed recall, Boston naming and Trails B scores as measures of specific domains in both groups of subjects. The number of errors on the American National Adult Reading Test was used as a measure of environmental enrichment provided by educational and occupational attainment, a component of cognitive reserve. We found that in cognitively normal subjects, none of the biomarkers correlated with the measures of cognition, whereas American National Adult Reading Test scores were significantly correlated with Boston naming and mini-mental state examination results. In cognitively impaired subjects, the American National Adult Reading Test and all biomarkers of neuronal pathology and amyloid load were independently correlated with all cognitive measures. Exceptions to this general conclusion were absence of correlation between cerebral spinal fluid amyloid-β1–42 and Boston naming and Trails B. In contrast, white matter hyperintensities were only correlated with Boston naming and Trails B results in the cognitively impaired. When all subjects were included in a flexible ordinal regression model that allowed for non-linear effects and interactions, we found that the American National Adult Reading Test had an independent additive association such that better performance was associated with better cognitive performance across the biomarker distribution. Our main conclusions included: (i) that in cognitively normal subjects, the variability in cognitive performance is explained partly by the American National Adult Reading Test and not by biomarkers of Alzheimer's disease pathology; (ii) in cognitively impaired subjects, the American National Adult Reading Test, biomarkers of neuronal pathology (structural magnetic resonance imaging and cerebral spinal fluid t-tau) and amyloid load (cerebral spinal fluid amyloid-β1–42) all independently explain variability in general cognitive performance; and (iii) that the association between cognition and the American National Adult Reading Test was found to be additive rather than to interact with biomarkers of Alzheimer's disease pathology.
PMCID: PMC3097887  PMID: 21478184
Alzheimer's disease; mild cognitive impairment; CSF biomarkers; MRI; cognitive reserve
5.  Linking Hippocampal Structure and Function to Memory Performance in an Aging Population 
Archives of neurology  2009;66(11):1385-1392.
Hippocampal atrophy and reductions in basal cerebral blood volume (CBV), a hemodynamic correlate of brain function, occur with cognitive impairment in Alzheimer's disease but whether these are early or late changes remains unclear. Magnetic resonance imaging (MRI) assesses structure and function in the hippocampal formation. The objective of the present study was to estimate differences in the associations of hippocampus and entorhinal cortex volumes and CBV with memory function in early and late stages of cognitive impairment by relating these measures with memory function in demented and nondemented persons with detailed brain imaging and neuropsychological assessment.
Design and Setting
Multivariate regression analyses were used to relate entorhinal cortex volume, entorhinal cortex CBV, hippocampus volume and hippocampus-CBV with measures of memory performance in 231 elderly persons from a community-based cohort. The same measures were related with language function as a reference cognitive domain.
There was no association between entorhinal cortex volume or hippocampus-CBV and memory. Decreased hippocampus volume was strongly associated with worse performance in total recall, while lower entorhinal cortex CBV was significantly associated with lower performance in delayed recall. Excluding persons with Alzheimer's disease (AD), the associations of entorhinal cortex CBV with memory measures was stronger, while the association between hippocampus volume and total recall became non-significant.
These finding suggest that in the early stages of AD or in nondemented persons with worse memory ability functional/metabolic hippocampal hypofunction contribute to memory impairment, while in the later stages both functional and structural changes play a role.
PMCID: PMC2778802  PMID: 19901171
entorhinal cortex cerebral blood volume; hippocampus volume; memory performance

Results 1-5 (5)