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• W2072310825 abstract "With different orders of magnitude, impairment in synaptic plasticity and neuronal integrity are observed both in “normal” aging and Alzheimer's disease (AD). Previous studies suggest that apolipoprotein E, the main lipoprotein carrier in the central nervous system, may be an important molecular modulator of both processes. Intriguingly, the presence/absence of apoE has been shown to differentially impact aging and AD: while cognitive deficits are observed in mice lacking apoE upon aging, the same genetic alteration alleviates amyloid pathology in AD transgenic models, thus eventually conferring a beneficial outcome towards the disease. Using novel in vivo methodological approaches, this study aims at further understanding how apoE modulates resilience and susceptibility of the neural system in both physiological and pathological contexts. In vivo calcium imaging in the visual cortex of awake animals, array tomography and conventional biochemical and histological approaches are performed to identify the functional and morphological consequences of apoE disruption on age- and AD-related neuronal dysfunction and synaptic changes. Our preliminary results suggest that apoE disruption impairs neuronal tuning for the direction of visual stimuli in adult wild-type mice (8-10 month old), resulting in an increased proportion of broadly tuned cells and a decreased number of highly tuned responders. This functional impairment is further amplified in APPPS1 AD transgenic mice when compared with wild-type, but the absence of apoE in those mice tends to improve this particular phenotype (the percentage of highly tuned cells in APPPS1/APOEKO animals reaches similar levels as APOEKO). The orientation selectivity index, however, remains unchanged between all the experimental groups (wt, APOEKO, APPPS, APPPS/APOEKO). Interestingly, the global amount of Abeta and the density of diffuse amyloid aggregates were not significantly different in APPPS and APPPS/APOEKO mice (even though a lower amount of dense-core fibrillar deposits was observed), therefore emphasizing on the role of apoE in modulating Abeta-related neuronal dysfunction rather than on amyloid deposition.In aged mice (18 month old), the presence of a higher percentage of “off-responders” was observed in APPPS compared with wild-type, APOEKO and APPPS/APOEKO animals, demonstrating that impairment of neuronal function may be specifically associated with the overexpression of AD-related genes and can be compensated by the absence of apoE. These results argue in favor of a complex role of apoE in maintaining neuronal function in a normal brain while alleviating amyloid-associated impairment of neuronal activity in aged transgenic mice. Further investigation of the synaptic profile of these different mouse lines will allow us to precisely associate our in vivo observations in awake living animals with changes in the distribution of pre- and post-synaptic elements, as well as changes in apoE-Abeta interactions." @default.
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• W2072310825 date "2014-07-01" @default.
• W2072310825 modified "2023-09-27" @default.
• W2072310825 title "O4-09-04: UNRAVELING THE ROLE OF APOLIPOPROTEIN E IN AGE- AND ABETA-RELATED NEURONAL DYSFUNCTION" @default.
• W2072310825 doi "https://doi.org/10.1016/j.jalz.2014.04.436" @default.
• W2072310825 hasPublicationYear "2014" @default.
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