Thursday, 21 August 2003
This presentation is part of : Thursday Poster Sessions

PD-075 The Distribution of Cerebral Amyloid Angiopathy within the Brain with Alzheimer's Disease May be Influenced by Apolipoprotein E4

Jinzhou Tian1, Jing Shi1, Corinne L Lendon2, Stuart M Pickering-Brown3, and David M A Mann4. (1) Department of Care of the Elderly, Beijing University of Chinese Medicine Dongzhimen Hospital, Beijing, China, (2) Department of Psychiatry, University of Birmingham, Birmingham, United Kingdom, (3) Department of Old Age Psychiatry, Institute of Psychiatry, London, United Kingdom, (4) Department of Medicine, University of Manchester, Manchester, United Kingdom

Objective: To investigate the association between the extent of cerebral amyloid angiopathy (CAA) and Apolipoprotein E (Apo E) e4 allele in Alzheimer's disease (AD).

Design: Mean comparison of two groups.

Materials and Methods: Brain tissues were obtained from 94 patients with autopsy confirmed AD. Apo E genotyping was determined from DNA extracted from frozen samples of frontal cortex or cerebellum using the polymerase chain reaction®Camplification technique. CAA was assessed on Weigert's haematoxylin-eosin stained sections in 4 brain regions (frontal cortex at Brodmann area 8/9, temporal cortex at Brodmann area 21/22, occipital cortex at Brodmann area 7/8, and parietal cortex at Brodmann area 39/40). One-way non-parametric analysis of variance ANOVA (SPSS) was applied to categorical variables when comparing differences in mean values across pathological or genotype groups. Mann-Whitney U test were used post hoc to identify significant differences between groups. Chi-square test was used to identify differences in frequency of affected cases within genotype groups. 2-tailed p values<=0.05 were considered statistically significant throughout all analyses.

Results: The mean total CAA scores summed across all 4 brain regions, and the mean scores within each region, did not differ either according to Apo E genotype, or between patients with 1, 2 or no ¶Ň4 alleles. However, once again there were significant differences in mean CAA score between the 4 brain areas according to Apo E genotype. The severity of CAA in occipital cortex in cases with Apo E ¶Ň4/¶Ň4 genotype (2.5+/-0.8) was significantly higher (p<0.05) than that in temporal (1.8+/-0.6) and parietal (1.9+/-1.1) cortex.

Conclusion: The likelihood of patients with AD suffering from CAA is not influenced by Apo E genotype, nor is the overall burden of the pathological change in the brain so influenced. However, the distribution of CAA within the brain with AD is at least partly influenced by genotype and dosage of Apo E ¶Ň4 allele, with the occipital cortex being more severely affected in those patients where Apo E ¶Ň4 allele is present.

Back to PD Thursday Poster Sessions
Back to The Eleventh International Congress