001     137945
005     20240321220338.0
024 7 _ |a 10.1371/journal.pone.0125418
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024 7 _ |a pmc:PMC4446269
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037 _ _ |a DZNE-2020-04267
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Jährling, Nina
|b 0
245 _ _ |a Cerebral β-Amyloidosis in Mice Investigated by Ultramicroscopy.
260 _ _ |a San Francisco, California, US
|c 2015
|b PLOS
264 _ 1 |3 online
|2 Crossref
|b Public Library of Science (PLoS)
|c 2015-05-27
336 7 _ |a article
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336 7 _ |a ARTICLE
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336 7 _ |a Journal Article
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520 _ _ |a Alzheimer´s disease (AD) is the most common neurodegenerative disorder. AD neuropathology is characterized by intracellular neurofibrillary tangles and extracellular β-amyloid deposits in the brain. To elucidate the complexity of AD pathogenesis a variety of transgenic mouse models have been generated. An ideal imaging system for monitoring β-amyloid plaque deposition in the brain of these animals should allow 3D-reconstructions of β-amyloid plaques via a single scan of an uncropped brain. Ultramicroscopy makes this possible by replacing mechanical slicing in standard histology by optical sectioning. It allows a time efficient analysis of the amyloid plaque distribution in the entire mouse brain with 3D cellular resolution. We herein labeled β-amyloid deposits in a transgenic mouse model of cerebral β-amyloidosis (APPPS1 transgenic mice) with two intraperitoneal injections of the amyloid-binding fluorescent dye methoxy-X04. Upon postmortem analysis the total number of β-amyloid plaques, the β-amyloid load (volume percent) and the amyloid plaque size distributions were measured in the frontal cortex of two age groups (2.5 versus 7-8.5 month old mice). Applying ultramicroscopy we found in a proof-of-principle study that the number of β-amyloid plaques increases with age. In our experiments we further observed an increase of large plaques in the older age group of mice. We demonstrate that ultramicroscopy is a fast, and accurate analysis technique for studying β-amyloid lesions in transgenic mice allowing the 3D staging of β-amyloid plaque development. This in turn is the basis to study neural network degeneration upon cerebral β-amyloidosis and to assess Aβ-targeting therapeutics.
536 _ _ |a 342 - Disease Mechanisms and Model Systems (POF3-342)
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542 _ _ |i 2015-05-27
|2 Crossref
|u http://creativecommons.org/licenses/by/4.0/
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650 _ 7 |a 1,4-bis(4'-hydroxystyryl)-2-methoxybenzene
|2 NLM Chemicals
650 _ 7 |a Alkenes
|2 NLM Chemicals
650 _ 7 |a Amyloid beta-Protein Precursor
|2 NLM Chemicals
650 _ 7 |a Benzene Derivatives
|2 NLM Chemicals
650 _ 7 |a Fluorescent Dyes
|2 NLM Chemicals
650 _ 7 |a Stilbenes
|2 NLM Chemicals
650 _ 2 |a Alkenes: analysis
|2 MeSH
650 _ 2 |a Alkenes: metabolism
|2 MeSH
650 _ 2 |a Amyloid beta-Protein Precursor: genetics
|2 MeSH
650 _ 2 |a Amyloidosis: pathology
|2 MeSH
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Benzene Derivatives: analysis
|2 MeSH
650 _ 2 |a Benzene Derivatives: metabolism
|2 MeSH
650 _ 2 |a Brain: pathology
|2 MeSH
650 _ 2 |a Disease Models, Animal
|2 MeSH
650 _ 2 |a Fluorescent Dyes: analysis
|2 MeSH
650 _ 2 |a Fluorescent Dyes: metabolism
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Imaging, Three-Dimensional: methods
|2 MeSH
650 _ 2 |a Mice, Inbred C57BL
|2 MeSH
650 _ 2 |a Mice, Transgenic
|2 MeSH
650 _ 2 |a Microscopy: methods
|2 MeSH
650 _ 2 |a Plaque, Amyloid: pathology
|2 MeSH
650 _ 2 |a Stilbenes
|2 MeSH
700 1 _ |a Becker, Klaus
|b 1
700 1 _ |a Wegenast-Braun, Bettina M
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700 1 _ |a Grathwohl, Stefan A
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700 1 _ |a Jucker, Mathias
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700 1 _ |a Dodt, Hans-Ulrich
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773 1 8 |a 10.1371/journal.pone.0125418
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773 _ _ |a 10.1371/journal.pone.0125418
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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913 1 _ |a DE-HGF
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|l Erkrankungen des Nervensystems
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914 1 _ |y 2015
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999 C 5 |9 -- missing cx lookup --
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|2 Crossref
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999 C 5 |9 -- missing cx lookup --
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|2 Crossref
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Marc 21