Poster Presentations: P3 P3-151
P685
COMPARING TRAJECTORIES OF GREY MATTER CHANGES IN ALZHEIMER’S DISEASE AND DEMENTIA WITH LEWY BODIES: A LONGITUDINAL STUDY
Elijah Mak1, Li Su1, Guy B. Williams2, Rosie Watson3, Michael Firbank4, Andrew M. Blamire5, John T. O’Brien1, 1University of Cambridge, Cambridge, United Kingdom; 2Wolfson Brain Imaging Centre, Cambridgeshire, United Kingdom; 3The Royal Melbourne Hospital, Melbourne, Australia; 4Newcastle University, Newcastle upon Tyne, United Kingdom; 5Newcastle University, Newcastle upon Tyne, United Kingdom. Contact e-mail:
[email protected] Background: The spatiotemporal patterns of grey matter changes in
dementia with Lewy bodies (DLB) remains poorly understood. Furthermore, while the longitudinal MRI technique has been established as a sensitive marker to track disease progression in Alzheimer’s disease, it has not been readily applied to DLB. Methods: We used FSL-SIENA and Freesurfer to quantify whole brain atrophy rates, rates of regional cortical thinning, and subcortical atrophy over 12 months in DLB (n¼13), compared to Alzheimer’s disease (AD) (n¼23) and healthy controls (HC) (n¼33). Subjects underwent both baseline and repeat MR imaging and clinical assessments within a 12-month interval. Results: At the whole brain level, AD had significantly greater volume loss over 12 months (-1.8%) compared to DLB (-1.0%; p ¼ 0.01) and HC (-0.9%; p < 0.01). Rates of temporal cortical thinning in DLB were relatively preserved compared to AD. At the subcortical level, AD group demonstrated significantly increased hippocampal atrophy (-5.8%) relative to the HC (-1.7%; p<0.001) and DLB groups
(-2.5%, p¼0.006) over 12 months. There was no significant difference in subcortical atrophy and ventricular expansion between DLB and HC. Conclusions: Overall, AD and DLB are characterized by different whole brain atrophy rates and spatiotemporal patterns of cortical thinning over time. DLB is characterized by a preservation of temporal regions relative to AD. Thus, besides validating the inclusion of the medial temporal lobe as a supportive biomarker in the revised diagnostic criteria for DLB, our findings also highlight the clinical utility of longitudinal cortical thinning as a complementary imaging marker to differentiate DLB from AD.
P3-152
CORRELATION BETWEEN METABOLIC AND CSF BIOMARKERS IN ALZHEIMER’S DISEASE PATIENTS WITH EARLY COGNITIVE DECLINE
Luka Jensterle1, Petra Tomse1, Uros Rot1, Andreja Emersic1, Zvezdan Pirtosek1, Chris C. Tang2, David Eidelberg2, Maja Trost1, 1 University Medical Centre Ljubljana, Ljubljana, Slovenia; 2The Feinstein Institute for Medical Research, Manhasset, NY, USA. Contact e-mail: maja.
[email protected] Background: Early diagnosis of Alzheimer’s dementia may be
difficult based on clinical presentation. Evaluation of different biomarkers can improve the diagnostic accuracy. We have recently utilized spatial covariance analysis with FDG/PET to identify a specific Alzheimer’s disease-related metabolic pattern (ADRP; attached Figure 1) that differentiates AD patients from healthy subjects (Mattis et al., 2015; manuscript in preparation). In this study, we aim to further evaluate the ability of ADRP expression to differentiate between patients with early cognitive disorder and normal controls (NC) and to correlate ADRP expression in individual subjects with their CSF biomarkers for Alzheimer’s disease. Methods: We studied 49 patients with early cognitive impairment (mean age 71.4 69.4 years, MMSE score 23.9 65.4, MoCA score 20.9 64.4) recruted from Center for cognitive disorders and 14 NC (mean age 64. 66.9 years, MMSE score 28.6 61.3, MoCA score 27.1 61.9). All subjects underwent lumbar puncture (amyloid b42 and p-tau were measured) as well as FDG/PET brain scan. An automated computational procedure was used to compute ADRP expression in the scans of individual subjects. ADRP scores were then used to separate between the AD and NC groups as well as correlate with amyloid beta/p-tau ratio. Results: The expression of ADRP was significantly increased in AD patients with cognitive impairment compared to normal controls (p¼0.003; Figure 2). ADRP