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Nat Med. 2014 Dec;20(12):1485-92. doi: 10.1038/nm.3734. Epub 2014 Nov 10.

Longitudinal PET-MRI reveals β-amyloid deposition and rCBF dynamics and connects vascular amyloidosis to quantitative loss of perfusion.

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Werner Siemens Imaging Center, Department of Preclinical Imaging and Radiopharmacy, Eberhard Karls University Tübingen, Tübingen, Germany.
Institute of Physiology II, Eberhard Karls University Tübingen, Tübingen, Germany.
Department of Cellular Neurology, Hertie-Institute for Clinical Brain Research, University of Tübingen, and DZNE, German Center for Neurodegenerative Diseases, Tübingen, Germany.
Synovo GmbH, Tübingen, Germany.
Target Discovery Research, Boehringer Ingelheim Pharma GmbH &Co. KG, Ingelheim, Germany.
Department of Nuclear Medicine, University of Leipzig, Leipzig, Germany.
Novartis Institutes for BioMedical Research, Basel, Switzerland.


The dynamics of β-amyloid deposition and related second-order physiological effects, such as regional cerebral blood flow (rCBF), are key factors for a deeper understanding of Alzheimer's disease (AD). We present longitudinal in vivo data on the dynamics of β-amyloid deposition and the decline of rCBF in two different amyloid precursor protein (APP) transgenic mouse models of AD. Using a multiparametric positron emission tomography and magnetic resonance imaging approach, we demonstrate that in the presence of cerebral β-amyloid angiopathy (CAA), β-amyloid deposition is accompanied by a decline of rCBF. Loss of perfusion correlates with the growth of β-amyloid plaque burden but is not related to the number of CAA-induced microhemorrhages. However, in a mouse model of parenchymal β-amyloidosis and negligible CAA, rCBF is unchanged. Because synaptically driven spontaneous network activity is similar in both transgenic mouse strains, we conclude that the disease-related decline of rCBF is caused by CAA.

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