Title |
Vascular and parenchymal amyloid pathology in an Alzheimer disease knock-in mouse model: interplay with cerebral blood flow
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Published in |
Molecular Neurodegeneration, August 2014
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DOI | 10.1186/1750-1326-9-28 |
Pubmed ID | |
Authors |
Hongmei Li, Qinxi Guo, Taeko Inoue, Vinicia A Polito, Katsuhiko Tabuchi, Robert E Hammer, Robia G Pautler, George E Taffet, Hui Zheng |
Abstract |
Accumulation and deposition of β-amyloid peptides (Aβ) in the brain is a central event in the pathogenesis of Alzheimer's disease (AD). Besides the parenchymal pathology, Aβ is known to undergo active transport across the blood-brain barrier and cerebral amyloid angiopathy (CAA) is a prominent feature in the majority of AD. Although impaired cerebral blood flow (CBF) has been implicated in faulty Aβ transport and clearance, and cerebral hypoperfusion can exist in the pre-clinical phase of Alzheimer's disease (AD), it is still unclear whether it is one of the causal factors for AD pathogenesis, or an early consequence of a multi-factor condition that would lead to AD at late stage. To study the potential interaction between faulty CBF and amyloid accumulation in clinical-relevant situation, we generated a new amyloid precursor protein (APP) knock-in allele that expresses humanized Aβ and a Dutch mutation in addition to Swedish/London mutations and compared this line with an equivalent knock-in line but in the absence of the Dutch mutation, both crossed onto the PS1M146V knock-in background. |
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Demographic breakdown
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Science communicators (journalists, bloggers, editors) | 1 | 100% |
Mendeley readers
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Demographic breakdown
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Researcher | 19 | 18% |
Student > Master | 12 | 12% |
Student > Bachelor | 11 | 11% |
Student > Doctoral Student | 8 | 8% |
Other | 13 | 13% |
Unknown | 20 | 19% |
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Pharmacology, Toxicology and Pharmaceutical Science | 4 | 4% |
Other | 16 | 15% |
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