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Abstract #2020

APPswe/PS1dE9 mice with cortical amyloid pathology show a reduced NAA/Cr ratio without apparent brain atrophy: A MRS and MRI study

Angela Kuhla1, Fatemah Sakr2, Claire Ruehlmann1, Tobias Lindner3, Stefan Polei3, Stefan Hadlich4, Bernd J Krause5, Brigitte Vollmar1, and Stefan Teipel2,6

1Institute for Experimental Surgery, Rostock University Medical Center, Rostock, Germany, 2Rostock University Medical Center, Rostock, Germany, 3Core Facility Multimodal Small Animal imaging, Rostock University Medical Center, Rostock University Medical Center, Rostock, Germany, 4Institute of Diagnostic Radiology & Neuroradiology, University Medicine Greifswald, Gerifswald, Germany, 5Department of Nuclear Medicine, Rostock University Medical Center, Rostock, Germany, 6German Center for Neurodegenerative Diseases (DZNE), Rostock, Germany

Amyloid-ß deposition is one of the hallmarks of Alzheimer’s disease (AD) that starts to progress decades before the onset of cognitive impairment. With the rise of the new diagnostic criteria of AD that considers the neuropathological changes as the main aspects for explaining the extent of the disease regardless the cognitive status of the patient & further highlighted the importance of finding reliable in-vivo biological markers to identify those in the preclinical stage of AD. Through the use of the transgenic mice models, particularly APPswe/PS1dE9 we could study the different pathomechanics contributing to the development of AD. So, in this study, we assumed an approach combining morphometry based on high-resolution MRI as a measure for the brain atrophy & proton magnetic resonance spectroscopy as a measure of neuronal functional viability. Then compare these data with a well known & standardized method as the histopathological assessments of neuron & amyloid plaques load. Using the quantitative neuroimaging allows us to translate these mechanistic findings in transgenic models to human phenotypes of brain morphology and function.

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