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@ARTICLE{Jhrling:137945,
author = {Jährling, Nina and Becker, Klaus and Wegenast-Braun,
Bettina M and Grathwohl, Stefan A and Jucker, Mathias and
Dodt, Hans-Ulrich},
title = {{C}erebral β-{A}myloidosis in {M}ice {I}nvestigated by
{U}ltramicroscopy.},
journal = {PLOS ONE},
volume = {10},
number = {5},
issn = {1932-6203},
address = {San Francisco, California, US},
publisher = {PLOS},
reportid = {DZNE-2020-04267},
pages = {e0125418},
year = {2015},
abstract = {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.},
keywords = {Alkenes: analysis / Alkenes: metabolism / Amyloid
beta-Protein Precursor: genetics / Amyloidosis: pathology /
Animals / Benzene Derivatives: analysis / Benzene
Derivatives: metabolism / Brain: pathology / Disease Models,
Animal / Fluorescent Dyes: analysis / Fluorescent Dyes:
metabolism / Humans / Imaging, Three-Dimensional: methods /
Mice, Inbred C57BL / Mice, Transgenic / Microscopy: methods
/ Plaque, Amyloid: pathology / Stilbenes /
1,4-bis(4'-hydroxystyryl)-2-methoxybenzene (NLM Chemicals) /
Alkenes (NLM Chemicals) / Amyloid beta-Protein Precursor
(NLM Chemicals) / Benzene Derivatives (NLM Chemicals) /
Fluorescent Dyes (NLM Chemicals) / Stilbenes (NLM
Chemicals)},
cin = {AG Jucker},
ddc = {610},
cid = {I:(DE-2719)1210001},
pnm = {342 - Disease Mechanisms and Model Systems (POF3-342)},
pid = {G:(DE-HGF)POF3-342},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:26017149},
pmc = {pmc:PMC4446269},
doi = {10.1371/journal.pone.0125418},
url = {https://pub.dzne.de/record/137945},
}