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| Home > Publications Database > Cerebral β-Amyloidosis in Mice Investigated by Ultramicroscopy. |
| Home > Publications Database > Cerebral β-Amyloidosis in Mice Investigated by Ultramicroscopy. |
| Journal Article | DZNE-2020-04267 |
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2015
PLOS
San Francisco, California, US
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Please use a persistent id in citations: doi:10.1371/journal.pone.0125418
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.
Keyword(s): Alkenes: analysis (MeSH) ; Alkenes: metabolism (MeSH) ; Amyloid beta-Protein Precursor: genetics (MeSH) ; Amyloidosis: pathology (MeSH) ; Animals (MeSH) ; Benzene Derivatives: analysis (MeSH) ; Benzene Derivatives: metabolism (MeSH) ; Brain: pathology (MeSH) ; Disease Models, Animal (MeSH) ; Fluorescent Dyes: analysis (MeSH) ; Fluorescent Dyes: metabolism (MeSH) ; Humans (MeSH) ; Imaging, Three-Dimensional: methods (MeSH) ; Mice, Inbred C57BL (MeSH) ; Mice, Transgenic (MeSH) ; Microscopy: methods (MeSH) ; Plaque, Amyloid: pathology (MeSH) ; Stilbenes (MeSH) ; 1,4-bis(4'-hydroxystyryl)-2-methoxybenzene ; Alkenes ; Amyloid beta-Protein Precursor ; Benzene Derivatives ; Fluorescent Dyes ; Stilbenes
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