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    Stabilized low-n amyloid-ß oligomers induce robust novel object recognition deficits associated with inflammatory, synaptic, and GABAergic dysfunction in the rat

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    McLean_Journal_of_Alzheimer's_Disease.pdf (991.7Kb)
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    Publication date
    2018-02
    Author
    Watremez, W.
    Jackson, J.
    Almari, B.
    McLean, Samantha L.
    Grayson, B.
    Neilla, J.C.
    Fischer, N.
    Allouche, A.
    Koziel, V.
    Pillot, T.
    Harte, M.K.
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    Keyword
    Alzheimer’s disease
    Amyloid-β oligomers
    Cognition
    Parvalbumin
    Interneurons
    Rights
    © 2018 IOS Press. Reproduced in accordance with the publisher's self-archiving policy. The final publication is available at IOS Press through http://dx.doi.org/10.3233/JAD-170489
    Peer-Reviewed
    Yes
    
    Metadata
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    Abstract
    Background:With current treatments for Alzheimer’s disease (AD) only providing temporary symptomatic benefits, disease modifying drugs are urgently required. This approach relies on improved understanding of the early pathophysiology of AD. A new hypothesis has emerged, in which early memory loss is considered a synapse failure caused by soluble amyloid-β oligomers (Aβo). These small soluble Aβo, which precede the formation of larger fibrillar assemblies, may be the main cause of early AD pathologies. Objective:The aim of the current study was to investigate the effect of acute administration of stabilized low-n amyloid-β1-42 oligomers (Aβo1-42) on cognitive, inflammatory, synaptic, and neuronal markers in the rat. Methods:Female and male Lister Hooded rats received acute intracerebroventricular (ICV) administration of either vehicle or 5 nmol of Aβo1-42 (10μL). Cognition was assessed in the novel object recognition (NOR) paradigm at different time points. Levels of inflammatory (IL-1β, IL-6, TNF-α), synaptic (PSD-95, SNAP-25), and neuronal (n-acetylaspartate, parvalbumin-positive cells) markers were investigated in different brain regions (prefrontal and frontal cortex, striatum, dorsal and ventral hippocampus). Results:Acute ICV administration of Aβo1-42 induced robust and enduring NOR deficits. These deficits were reversed by acute administration of donepezil and rolipram but not risperidone. Postmortem analysis revealed an increase in inflammatory markers, a decrease in synaptic markers and parvalbumin containing interneurons in the frontal cortex, with no evidence of widespread neuronal loss. Conclusion:Taken together the results suggest that acute administration of soluble low-n Aβo may be a useful model to study the early mechanisms involved in AD and provide us with a platform for testing novel therapeutic approaches that target the early underlying synaptic pathology.
    URI
    http://hdl.handle.net/10454/15087
    Version
    Accepted Manuscript
    Citation
    Watremez W, Jackson J, Almari B et al (2018) Stabilized low-n amyloid-ß oligomers induce robust novel object recognition deficits associated with inflammatory, synaptic, and GABAergic dysfunction in the rat. Journal of Alzheimer’s Disease. 62(1): 213-226.
    Link to publisher’s version
    http://dx.doi.org/10.3233/JAD-170489
    Type
    Article
    Collections
    Life Sciences Publications

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