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

Florian Maier | Zendy; Hans F. Wehrl | Zendy; Andreas M. Schmid | Zendy; Julia G. Mannheim | Zendy; Stefan Wiehr | Zendy; Chommanad Lerdkrai | Zendy; Carsten Calaminus | Zendy; Anke Stahlschmidt | Zendy; Lan Ye | Zendy; Michael Burnet | Zendy; Detlef Stiller | Zendy; Osama Sabri | Zendy; Gerald Reischl | Zendy; M Staufenbiel | Zendy; Olga Garaschuk | Zendy; Mathias Jucker | Zendy; Bernd J. Pichler | Zendy

Open Access

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

Author(s) -

Florian Maier,

Hans F. Wehrl,

Andreas M. Schmid,

Julia G. Mannheim,

Stefan Wiehr,

Chommanad Lerdkrai,

Carsten Calaminus,

Anke Stahlschmidt,

Lan Ye,

Michael Burnet,

Detlef Stiller,

Osama Sabri,

Gerald Reischl,

M Staufenbiel,

Olga Garaschuk,

Mathias Jucker,

Bernd J. Pichler

Publication year - 2014

Publication title -

nature medicine

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 19.536

H-Index - 547

eISSN - 1546-170X

pISSN - 1078-8956

DOI - 10.1038/nm.3734

Subject(s) - cerebral amyloid angiopathy , amyloidosis , pittsburgh compound b , amyloid (mycology) , cerebral blood flow , pathology , positron emission tomography , magnetic resonance imaging , perfusion , alzheimer's disease , genetically modified mouse , in vivo , medicine , neuroscience , disease , biology , transgene , dementia , radiology , biochemistry , microbiology and biotechnology , gene

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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