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P1–319: The impact of beta‐amyloid deposition and vascular risk factors on cortical thickness and cognition
Author(s) -
Villeneuve Sylvia,
Reed Bruce,
Madison Cindee,
Wirth Miranka,
Kriger Stephen,
Haase Claudi M.,
Marchant Natalie,
Decarli Charles S.,
Chui Helena,
Weiner Michael,
Jagust William
Publication year - 2013
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 - 10.1016/j.jalz.2013.05.545
Subject(s) - medicine , framingham risk score , diabetes mellitus , cardiology , risk factor , cognitive decline , psychology , dementia , endocrinology , disease
Background: Vascular risk factors are suspected to play a role in the etiology of Alzheimer’s disease. Recently, a model that relates capillary dysfunction to the development of AD was proposed [1]. The model predicts that increased capillary dysfunction leads to increased oxygen extraction in order to support the metabolic requirements of the brain tissues. In this study we investigated the brain oxygen extraction capacity (OEF max) in AD patients and controls using dynamic susceptibility contrast (DSC) magnetic resonance imaging (MRI). Methods: Eighteen (13 females) patients with clinically suspected possible or probable AD verified by ICD-10, DSMIV, and NINCDS-ADRDA (MMSE: 24.562.7, age: 72.965.1) and 19 (8 females) cognitively normal (MMSE 28) age-matched (age: 67.166.4) and healthy controls were scanned using DSC and T1-weighted (T1w) MRI. OEF max maps, modeled under the assumption of a fixed tissue oxygen tension, were calculated from the perfusion images using a parametric deconvolution method [2] and parcellated using the T1w images and an atlas-based method [3]. Brain atrophy was estimated by cortical thickness [4] and hippocampal volume [5] automatically calculated from the T1w images. Differences between AD patients and controls were determined using two-tailed t-tests. Results: No differences were found in whole brain OEF max between AD patients and controls (p1⁄40.282). Significantly higher OEF in AD patients was found in right putamen (p1⁄40.042) and right thalamus (p1⁄40.044). Areas with lower OEF in AD patients were not detected. Hippocampal volumes were smaller in AD patients (left: p1⁄40.010, right: p1⁄40.009) and significant cortical thinning was found bilaterally in the precuneus, the cingulate (primarily posterior), and large parts of the temporal and frontal lobes indicating widespread atrophy. Conclusions: Increased OEF max was detected in basal ganglia and thalamus in AD patients compared to controls. These findings are consistent with the capillary dysfunction hypothesis of AD. The widespread cortical atrophy and smaller hippocampal volumes in the AD patients suggest pathologies of late Braak stages. Further studies should address the causal relation between elevated OEFmax and atrophy. References: [1]Ostergaard et al., Neurobiology of aging, 2013. 34(4):1018-31. [2]Mouridsen et al., ISMRM 2011. [3]Fonov et al.,NeuroImage, 2011. 54(1):313-27. [4]Eskildsen et al., MICCAI 2006. [5]Coupe et al., NeuroImage, 2012. 59(4):3736-47.