IC‐P‐052: Amyloid Levels in Cerebral Spinal Fluid Influences The Pattern of Cortical and Basal Forebrain Atrophy in Mild Cognitive Impairment
Article 2016 en
Authors
IK
Ingo Kilimann
PS
Petr Sabik
LH
Lucrezia Hausner
Abstract
1 min read
The basal forebrain cholinergic system (BFCS) is the main source of acetylcholine for the neocortex. The BFCS is early affected in Alzheimer's disease (AD), and atrophy can be seen already in pre-dementia stages. In these stages, CSF levels of amyloid are accepted to be a good marker for AD pathology. We analysed the effect of amyloid on BFCS, in addition the pattern of hippocampal atrophy and cortical thickness. We used structural imaging data from the European DTI study in dementia (EDSD). We analyzed the cortical thickness from MRIs of 64 individuals with mild cognitive impairment (MCI) – a risk state of AD - and 62 cognitively healthy elderly controls (HC) using FreeSurfer Software. Furthermore, we applied voxel-based morphometry for BFCS and hippocampus volumetric measures. All MCI individual underwent lumbar puncture and were tested for ß-amyloid levels. Using cut-off levels for amyloid from local labs, the MCI (all, MCIa) group was split in an amyloid positive (MCI+) and amyloid negative group (MCI-). We found differences in the pattern of correlations between cortical thickness and BFCS subregions in the healthy controls group and the MCIa group. The MCIa group showed a significant correlation along the know projections between cortical thickness of the temporal region and the volume of the Ch4p region. This association was not found in the HC group. Taking CSF amyloid status in account, only the MCI+ group showed a significant association between the atrophy in the posterior parts of the BFCS like the nucleus basalis Meynert (Ch4) and temporal cortex. The hippocampus volume also showed only in the MCI+ group significant correlations to the temporal cortical thickness. The amyloid status in MCI patients influences the topography of BFCS atrophy and cortical thinning, which underlines the possible differences of pathophysiology of amyloid-related and non-related cognitive impairment.
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