1. Longitudinal PET-MRI reveals β-amyloid deposition and rCBF dynamics and connects vascular amyloidosis to quantitative loss of perfusion
- Author
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Chommanad Lerdkrai, Mathias Jucker, Carsten Calaminus, Hans F. Wehrl, Andreas Schmid, Detlef Stiller, Lan Ye, Gerald Reischl, Olga Garaschuk, Mathias Staufenbiel, Stefan Wiehr, Julia G. Mannheim, Anke Stahlschmidt, Osama Sabri, Bernd J. Pichler, Florian C. Maier, and Michael Burnet
- Subjects
Pathology ,2-(4'-(methylamino)phenyl)-6-hydroxybenzothiazole ,Perfusion scanning ,Plaque, Amyloid ,Multimodal Imaging ,Amyloid beta-Protein Precursor ,Mice ,pathology [Brain] ,Longitudinal Studies ,metabolism [Cerebral Amyloid Angiopathy] ,Aniline Compounds ,pathology [Cerebral Hemorrhage] ,medicine.diagnostic_test ,Amyloidosis ,Brain ,General Medicine ,Magnetic Resonance Imaging ,diagnostic imaging [Cerebral Amyloid Angiopathy] ,Cerebral blood flow ,genetics [Amyloid beta-Protein Precursor] ,Positron emission tomography ,Cerebrovascular Circulation ,Female ,Cerebral amyloid angiopathy ,Perfusion ,medicine.medical_specialty ,Perfusion Imaging ,metabolism [Amyloid beta-Peptides] ,Mice, Transgenic ,pathology [Cerebral Amyloid Angiopathy] ,General Biochemistry, Genetics and Molecular Biology ,medicine ,Animals ,ddc:610 ,pathology [Plaque, Amyloid] ,Benzothiazoles ,Beta (finance) ,diagnostic imaging [Brain] ,Cerebral Hemorrhage ,Amyloid beta-Peptides ,business.industry ,Magnetic resonance imaging ,diagnostic imaging [Cerebral Hemorrhage] ,medicine.disease ,metabolism [Plaque, Amyloid] ,Cerebral Amyloid Angiopathy ,Disease Models, Animal ,Thiazoles ,metabolism [Brain] ,Positron-Emission Tomography ,diagnostic imaging [Plaque, Amyloid] ,Radiopharmaceuticals ,business - Abstract
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.
- Published
- 2013
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