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Enhanced Cerebral Blood Volume under Normobaric Hyperoxia in the J20-hAPP Mouse Model of Alzheimer’s Disease

View ORCID ProfileOsman Shabir, Paul Sharp, Monica A Rebollar, Luke Boorman, Clare Howarth, Stephen B Wharton, Sheila E Francis, View ORCID ProfileJason Berwick
doi: https://doi.org/10.1101/848713
Osman Shabir
1The Neurovascular & Neuroimaging Group (Department of Psychology), University of Sheffield (Sheffield, United Kingdom)
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  • ORCID record for Osman Shabir
Paul Sharp
1The Neurovascular & Neuroimaging Group (Department of Psychology), University of Sheffield (Sheffield, United Kingdom)
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Monica A Rebollar
2Sheffield Institute for Translational Neuroscience (SITraN), University of Sheffield (Sheffield, United Kingdom)
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Luke Boorman
1The Neurovascular & Neuroimaging Group (Department of Psychology), University of Sheffield (Sheffield, United Kingdom)
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Clare Howarth
1The Neurovascular & Neuroimaging Group (Department of Psychology), University of Sheffield (Sheffield, United Kingdom)
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Stephen B Wharton
2Sheffield Institute for Translational Neuroscience (SITraN), University of Sheffield (Sheffield, United Kingdom)
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Sheila E Francis
3Department of Infection, Immunity & Cardiovascular Disease (IICD), University of Sheffield (Sheffield, United Kingdom)
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Jason Berwick
1The Neurovascular & Neuroimaging Group (Department of Psychology), University of Sheffield (Sheffield, United Kingdom)
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  • For correspondence: j.berwick@sheffield.ac.uk
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Abstract

Early impairments to neurovascular coupling have been proposed to be a key pathogenic factor in the onset and progression of Alzheimer’s disease (AD). Studies have shown impaired neurovascular function in several mouse models of AD, including the J20-hAPP mouse. In this study, we aimed to investigate early neurovascular changes using wild-type (WT) controls and J20-hAPP mice at 6-9 months of age, by measuring cerebral haemodynamics and neural activity to physiological sensory stimulations. A thinned cranial window was prepared to allow access to cortical vasculature and imaged using 2D-optical imaging spectroscopy (2D-OIS). After chronic imaging sessions where the skull was intact, a terminal acute imaging session was performed where an electrode was inserted into the brain to record simultaneous neural activity. We found that cerebral haemodynamic changes were significantly enhanced in J20-hAPP mice compared with controls in response to physiological stimulations, potentially due to the significantly higher neural activity (hyperexcitability) seen in the J20-hAPP mice. Thus, neurovascular coupling remained preserved under a chronic imaging preparation. Further, under hyperoxia, the baseline blood volume and saturation of all vascular compartments in the brains of J20-hAPP mice were substantially enhanced compared to WT controls, but this effect disappeared under normoxic conditions. This study highlights novel findings not previously seen in the J20-hAPP mouse model, and may point towards a potential therapeutic strategy by driving an increased baseline blood flow to the brain, thereby potentially enhancing the clearance of beta-amyloid.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-ND 4.0 International license.
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Posted November 19, 2019.
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Enhanced Cerebral Blood Volume under Normobaric Hyperoxia in the J20-hAPP Mouse Model of Alzheimer’s Disease
Osman Shabir, Paul Sharp, Monica A Rebollar, Luke Boorman, Clare Howarth, Stephen B Wharton, Sheila E Francis, Jason Berwick
bioRxiv 848713; doi: https://doi.org/10.1101/848713
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Enhanced Cerebral Blood Volume under Normobaric Hyperoxia in the J20-hAPP Mouse Model of Alzheimer’s Disease
Osman Shabir, Paul Sharp, Monica A Rebollar, Luke Boorman, Clare Howarth, Stephen B Wharton, Sheila E Francis, Jason Berwick
bioRxiv 848713; doi: https://doi.org/10.1101/848713

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