alexa Cerebral Glucose Transport And Blood-brain Barrier Morphology Are Altered In Function Of Apolipoprotein E Genotype In Mice
ISSN: 2161-0460

Journal of Alzheimers Disease & Parkinsonism
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2nd International Conference on Alzheimers Disease and Dementia
September 23-25, 2014 Valencia Convention Centre, Spain

Wael Alata, Milene Vandal and Frederic Calon
Accepted Abstracts: J Alzheimers Dis Parkinsonism
DOI: 10.4172/2161-0460.S1.010
Abstract
The blood-brain barrier (BBB) is a dynamic and biological barrier, which physically separates the blood from the central nervous system (CNS). Several studies suggest that changes in the BBB occur in Alzheimer?s disease (AD). Among the three common isoforms of apolipoprotein E (ApoE, alleles ?2, ?3 or ?4), the expression of the ?4 allele is a major genetic risk factor for AD. We hypothesized that ?4 allele exerts a pathogenic role by affecting the functional and morphological properties of the BBB. Using the quantitative in situ brain perfusion technique, we first found lower (13.0 - 17.0%) brain transport coefficient (Clup) of [3H]-diazepam in APOE4 mice at 4 and 12 months, compared to APOE2 and APOE3 mice, reflecting a decrease of cerebral vascularization. Accordingly, results from immunofluorescence experiments revealed reduced cerebral vessel density (26 and 38%) and thinner basement membrane (30 and 35%) in 12-month-old APOE4 mice compared to APOE2 and APOE3 mice, suggesting vascular atrophy. In addition, APOE4 mice displayed a 29% reduction of [3H]-D-glucose transport through the BBB compared to APOE2 mice without significant changes in the expression of its transporter GLUT1 in brain capillaries. However, an increase of 41.3% of RAGE was found in brain capillaries of 12-month-old APOE4 mice compared to APOE2 without significant changes of LRP1. In conclusion, profound divergences were observed between APOE genotypes at the cerebrovascular interface. Further investigations are needed to determine whether these allele-specific BBB anomalies contribute to the development of AD.
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