the synthesis of NGF and calcium channels. VDR gene polymorphisms can be related with neurodegenerative diseases and neuronal damage. Objec- tive(s): In this study, our aim was to determine if there is an association between VDR gene and late-onset AD. Methods: Eigthy-four cases of dementia of Alzheimer type and 84 age-matched controls (mean ages 74.7, and 72.2 years, respectively) have been included in the study. Patients are clinically diagnosed according to DSM-IV criterias. We used PCR and RFLP to test for an association between AD and ApaI and TaqI polymor- phisms at VDR gene. Results: When the controls and patients were compared for their TaqI genotype a nearly significant difference was observed (p=0.07). On the other hand when the ApaI genotypes compared, the frequency of the patients with Aa genotype observed significantly higher than the frequency of the healthy individuals with the same geno- type (p=0.0018). Conclusions: We concluded that having “Aa” genotype may increase the risk of developing AD 3 times when compared with having “AA” (p=0.00075, OR=3.05, 95% CI 1.583-5.907). With the AA genotype as a reference the Aa+aa together was associated with a 2.5 times increased in risk of AD (p=0.003, OR=2.574, 95% CI 1.370-4.837). P1-337 MAPPING OF NEURONATOMICAL CHANGES ASSOCIATED WITH APOE GENOTYPE IN ALZHEIMER’S DISEASE Harald Hampel 1 , Michael Ewers 1 , Christine Born 2 , Schoenberg O. Stefan 2 , Stefan J. Teipel 1 , 1 Dementia and Neuroimaging Research Section, Alzheimer Memorial Center and Geriatric Psychiatry Branch, Department of Psychiatry, Ludwig-Maximilian University, Munich, Germany; 2 Department of Clinical Radiology, University Hospital of Munich, Ludwig-Maximilian University, Munich, Germany. Contact e-mail: Michael.Ewers@med.uni-muenchen.de Background: The epsilon 4 allele of the apolipoprotein-E (ApoE) gene is a major risk factor of Alzheimer’s disease (AD). Multiple MRI-based studies have shown that the presence of the ApoE 4 allele is associated with increased volumetric loss within the hippocampus and amygdala. However, the spatial pattern of neuronatomical changes within the whole brain associated with ApoE genotpype in AD is well known. Objective(s): To assess the spatial pattern of cerebral volumetric differences between ApoE carriers and ApoE non-carriers in AD. Methods: A total 58 patients with Alzheimer’s disease including 34 ApoE-4 carriers (ApoE 3/4: n = 26, ApoE 4/4: n = 8) and 24 ApoE non-carriers (3/3) were scanned on a 1.5 Tesla scanner. MRI scans were normalized to a customized group-specific grey matter template prior to statistical analysis, using the program SPM2. Group differences in grey matter volume were tested voxel-by-voxel in an ANCOVA with global grey matter volume as a covariate, using a significance threshold of  = 0.001. The mean MMSE was 24.3 (SD = 3.8) for ApoE-4 non-carriers and 24.1 (SD = 2.9) for ApoE-4 carriers. The groups did not differ in age, gender, education, and duration of disease. Results: Results showed a decrease in grey matter volume primarily within the left hippocampus, amydala and parahippocampal gyrus in ApoE-4 carriers. In contrast, a relative increase in grey matter volume was observed primarily within the dorso-lateral prefrontal cortex, precentral gyrus, and inferior parietal lobule. Conclusions: ApoE-4 genotype is associated with a region-dependent increase and decrease in grey matter volume in AD. Future studies need to investigate whether the increase of grey matter volume observed within the fronto-parietal brain regions in ApoE-4 carriers may underlie potential compensatory processes associated with ApoE 4. P1-338 APOLIPOPROTEIN E GENOTYPE IN DEMENTED AND NON-DEMENTED CENTENARIANS Maria Styczyn ´ ska 1 , Beata Peplon ´ska 1 , Dorota Religa 1,2 , Anna Pfeffer 1 , Malgorzata Chodakowska-ebrowska 3 , Eløbieta £uczywek 1 , Anna Barczak 3 , Aleksandra Szybin ´ska 4 , Katarzyna Broczek 4 , Malgorzata Kobryœ 1 , Maria Barcikowska 1 , 1 Medical Research Center, Polish Academy of Sciences, Warszawa, Poland; 2 Karolinska Institutet, Stockholm, Sweden; 3 MSWiA Hospital, Warszawa, Poland; 4 International Institute of Molecular and Cell Biology, Warszawa, Poland. Contact e-mail: desperat@cmdik.pan.pl Background: The most common type of dementia is the late-onset, spo- radic Alzheimer’s disease (AD), a progressive neurodegenerative disorder with complex pathogenesis. It is widely recognized that the prevalence of dementia increases exponentially as we get older. Among the genetic factors that contribute to the development of AD, apolipoprotein E (APOE) polymorphism is the most important one. As our earlier study showed, the frequency of APOE e4 allele in Polish patients with Alzheimer’s disease aged about 70 years was 0.325, whereas in the age-matched control group it was 0.11 (p0.005). Objective: The aim of this study was to check the distribution of APOE alleles in Polish centenarians and to look for the differences between the demented and the non-demented subjects. Meth- ods: The study group consisted of 74 Polish centenarians examined by a neurologist. Forty nine cases (66%) were diagnosed with dementia (based on interviews and evaluations in MMSE and GDS scales). APOE geno- typing was done using PCR-RFLP method. Results: The frequencies of APOE e4, e3 and e2 alleles in the whole group were 0.033, 0.824 and 0.142, respectively. There were no statistically significant differences be- tween the frequency of APOE e4 allele in the demented and the non- demented centenarians (0.04 vs 0.02), but both frequencies were signifi- cantly lower than the ones observed in AD patients and the healthy population aged 70 y. Conclusions: Our findings show that APOE geno- type does not increase the chance of dementia in the oldest old. The much lower percentage of APOE e4 allele in this group compared with the one in the younger population suggests that it may influence the mortality rate. P1-339 MTDNA INHERITED AND SOMATIC VARIABILITY IN ALZHEIMER’S DISEASE Aurelia Santoro 1 , Elisa Balducci 1 , Francesca Rosini 1 , Alberto Montesanto 2 , Stefano Salvioli 1 , Giuseppina Rose 2 , Elena Bellavista 1 , Michele Mishto 1 , Elena Bonora 1 , Giuseppe Gasparre 1 , Andrea Chiamenti 3 , Giovanna De Benedictis 2 , Giovanni Romeo 1 , Carlo Gabelli 3 , Tilman Grune 4 , Gaetano Crepaldi 5 , Claudio Franceschi 1 , 1 University of Bologna, Bologna, Italy; 2 University of Calabria, Rende (CS), Italy; 3 Regional Center for Cerebral Aging, Vicenza, Italy; 4 Research Institute of Environmental Medicine, Duesseldorf, Germany; 5 University of Padova, Padova, Italy. Contact e-mail: aurelia.santoro@unibo.it Sporadic Alzheimer’s Disease (AD), the late onset form of AD, is a complex disease in which several susceptibility genes interact with each other and with environmental factors, in modulating the risk to develop AD. Oxidative stress and mitochondria are hypothesized to play a major role in AD onset and progression. We investigated the role of mitochondrial DNA (mtDNA) in AD, evalu- ating mitochondrial inherited variability (haplogroups) and its possible interaction with APOE, a nuclear gene well known as risk factor for AD, as well as mitochondrial somatic variability (accumulation of mutations). We investigated the association of mtDNA haplogroups with AD in a case-control study on 237 AD patients and 237 age-matched controls from the Veneto region. Male AD patients with haplogroups U and K appear to protect (O.R.: 0,403; 95% CI: 0,167-0,970; p= 0,043), while those with haplogroups H and V appear to have an increased AD risk (O.R.: 1,953; 95% CI: 1,013-3,767; p=0,046). In female patients no correlation between mtDNA haplogroups and disease was found. In both groups (male and female AD patients) no correlation between mtDNA haplogroups and APOE gene variants was found. Moreover, the accumulation of sporadic mutations was analyzed by resequencing the entire mtDNA molecule (16.569 bp) in two brain areas (hippocampus and cerebellum) from 10 AD patients and in the hippocampus of 9 age-matched non AD affected controls. The analysis of the mtDNA sequences showed a significant prevalence of heteroplasmic mutations in the hippocampus from AD pa- tients in comparison with cerebellum (a brain area much less affected by S196 Poster Presentations P1