measured by applying registration and the Boundary Shift Integral (BSI) to longitudinal MRI. The initial stage of BSI calculation typically involves time-consuming semi-automated delineation of brain on baseline and repeat scans. Automated propagation of the baseline brain region onto the repeat scan has been suggested as a method to reduce operator time. This study compares the performance, in terms of BSI values, of a novel automated propagation method with semi-automatic segmentation based on BSI values. Methods: Twenty-five AD, 74 MCI and 54 control subjects were selected from the Alzheimer’s Disease Neuroimaging Initiative cohort, each with a volumetric, T1-weighted 1.5T scan at baseline and 12 months. Scans from both time points were first semi-automatically segmented, with a threshold-based technique. The baseline scan was then registered to the repeat using both affine and freeform registration and the derived registration parameters were used to transform the baseline region to the repeat image. Morphological operations (1 erosion, 2 conditional dilations) were applied to improve boundary location. Finally, whole-brain BSIs were calculated for each subject by registering the semi-automatically segmented repeat and the automatically segmented (prop- agated) repeat separately to the baseline. Agreement between the resulting semi-automatic and propagated BSIs was calculated by plotting the 95% levels (1.96 std). Results: Limits of agreement were found to be narrow: for 95% of cases, propagated BSIs were between 0.108% greater and 0.128% lower than the semi-automated method (figure). There was a slight but significant bias (p0.05) with semi-automated BSIs being 0.01% of brain volume higher; this is much lower than the BSI scan-rescan reproducibility (0.2%) and very much lower than typical annual brain atrophy in AD (2%). For low/negative rates of atrophy the semi-automated BSI tends to be slightly smaller than propagated, and for larger rates the semi-automated BSI tends to be larger. Conclusions: Although there is a small degree of bias the propagation method is comparable to the conventional semi-automated methods in terms of the BSI result and saves operator time. P2-008 REGIONAL GRAY MATTER BRAIN VOLUME DIFFERENCES IN INDIVIDUALS WITH A MATERNAL VERSUS PATERNAL FAMILY HISTORY OF ALZHEIMER’S DISEASE Michele E. Fitzgerald 1,2 , Barbara B. Bendlin 1,2 , Donald G. McLaren 1,2 , Guofan Xu 1,2 , Erik K. Kastman 1,2 , Lisa M. Newman 1,2 , Sanjay Asthana 1,2 , Mark A. Sager 1 , Sterling C. Johnson 1,2 , 1 Univsersity of Wisconsin - Madison, Madison, WI, USA; 2 William S. Middleton VA Hospital, Madison, WI, USA. Contact e-mail: gxu@medicine.wisc.edu Background: First-degree family history of Alzheimer’s disease (AD) is a known risk factor for developing AD. Recently Mosconi, et al., 2007 found that individuals with a maternal family history (FHm) of AD show cerebral metabolic rate of glucose (CMRglc) reductions in brain regions affected in AD patients compared to individuals with a paternal family history (FHp) and those without a parental history (FH - ). The present study examined differences in regional gray matter volume (GMV) between FHm, FHp and FH - groups. Based on Mosconi’s results, we hypothesized that the FHm group would show lower GMV compared to the FHp and FH - groups in regions vulnerable to AD (medial temporal lobe, posterior cingulate cortex (PCC), parietotemporal and frontal cortices). Methods: A voxel-based morphometry analysis was per- formed to assess regional GMV differences in 197 cognitively normal adults (aged 40 -65): 80 FHm, 44 FHp, 73 FH - . Groups were matched on age, sex, education, and prevelance of apolipoprotein E 4 allele. T1-weighted magnetic resonance images (MRI) were acquired on a 3T scanner. Gray matter proba- bility maps were generated by segmenting, normalizing and smoothing the MRIs using the VBM5 toolbox in SPM5. An ANOVA was performed with the gray matter probability maps, controlling for sex, age, education and total GMV. Results: The FHm group showed lower GMV in the PCC and the right inferior parietal lobule (P=.001 unc.) compared to the FHp group, while the FHp group showed lower GMV in the right parahippocampal gyrus (P=.001 unc) compared to the FHm group. When restricted to these regions, compar- isons with the FH - group revealed higher GMV in the right parahippocampal gyrus in the FHm group and higher GMV in the PCC in the FHp group (P=.001 unc). Conclusions: These results show that FHm and FHp risk factors differentially affect GMV in brain regions vulnerable to AD. Further, the higher GMV observed in the at-risk groups was inconsistent with our hypothesis. Whether this result suggests a pathological or compensatory mech- anism requires further investigation. P2-009 CHARACTERISATION OF [ 18 F]-BF227 BINDING TO -SYNUCLEIN Michelle Fodero-Tavoletti 1,2 , Rachel Mulligan 3 , Nobuyuki Okamura 4 , Shozo Furumoto 5 , Christopher C. Rowe 3 , Yukitsuka Kudo 5 , Colin L. Masters 6 , Roberto Cappai 1,2 , Kazuhiko Yanai 4 , Victor L. Villemagne 3,6 , 1 University of Melbourne, Dept Pathology, Melbourne, Australia; 2 Bio21 Institute, Melbourne, Australia; 3 Centre for PET, Austin Health, Melbourne, Australia; 4 Tohoku University, Dept Pharmacology, Sendai, Japan; 5 Tohoku University, Biomedical Engineering Research Organization, Sendai, Japan; 6 The Mental Health Research Institute, Melbourne, Australia. Contact e-mail: m.fodero@unimelb.edu.au Background: A accumulation in plaques is one of the pathological hall- marks of Alzheimer’s disease (AD), but also occurs in Dementia with Lewy Bodies (DLB). [ 11 C]-PiB-PET studies have shown a similar pattern of [ 11 C]- PiB retention as seen in AD. Since [ 18 F]-BF227 shares some structural simi- larities to [ 11 C]-PIB, we characterised the in vitro binding properties of [ 18 F]- BF227 to A 1-42 and -synuclein fibrils and AD, pure DLB and control brain homogenates, to investigate whether [ 18 F]-BF227 binds to Lewy bodies (LB), in addition to A plaques. Methods: In vitro saturation studies with 0.1-250 nM [ 18 F]-BF227 were carried out on either 200 nM -syn or A 42 fibrils or 100g of AD, pure DLB or control brain homogenates. Non-specific binding was established with PiB (1M). Results: In vitro binding assays indicated that [ 18 F]-BF227 binds to A 1-42 fibrils in a saturable manner and exhibited affinities in the nanomolar range (K D =5.50.5 nM), while the K D for -syn was (K D =3.80.5 nM). Furthermore, [ 18 F]-BF227 was observed to bind to A plaque-containing AD brain homogenates with high affinity (K D =250.5 nM), but failed to bind to A plaque-free DLB (“pure DLB”) or age-matched control homogenates. Conclusions: In vitro binding studies suggest that [ 18 F]- BF227 is not selective for A. Evaluation of BF227 in Parkinson’s disease using midbrain homogenates is warranted P2-010 DOES VARIABLE PROGRESSION OF INCIDENTAL WHITE MATTER HYPERINTENSITIES IN ALZHEIMER’S DISEASE RELATE TO VENOUS INSUFFICIENCY? Fuqiang Gao, Stephen van Gaal, Naama Levy-Cooperman, Joel Ramirez, Christopher J. M. Scott, June Bilbao, Sandra E. Black, Sunnybrook Health Science Center, University of Toronto, Toronto, ON, Canada. Contact e-mail: fuqiang.gao@sw.ca Background: Incidental white matter hyperintensities (WMH) in Alzheimer’s disease (AD) are usually attributed to small arterial occlusive disease. How- ever, variability in lesion change over time and unpredictable conditions T368 Poster Presentations P2