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      Morphologic and biometric evaluation of chick embryo eyes in ovo using 7 Tesla MRI

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          Abstract

          The purposes of this study were (1) to characterize embryonic eye development during incubation in ovo and (2) to analyze the putative influence of repetitive ultrahigh-field MRI (UHF-MRI) measurements on this development. A population of 38 fertilized chicken eggs was divided into two sub-groups: two eggs (Group A) were examined repeatedly during the developmental period from embryonic day 1 (E1) to embryonic day 20 (E20) to evaluate the influence of daily MRI scanning. A second larger group of 36 eggs was examined pairwise on one day only, from E3 to E20, and the embryos were sacrificed immediately after MR imaging (Group B). Fast T2-weighted MR sequences provided biometric data on the eye with an in-plane resolution of 74 μm. The data show rapid growth of the eye with a steep increase in intraocular dimensions in all axis directions and in eyeball volume during initial development up to E10, followed by a phase of reduced growth rate in later developmental stages. Comparison of the two groups revealed no differences in ocular development.

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          A series of normal stages in the development of the chick embryo

          Viktor Hamburger, Howard L. Hamilton (1951)
          Article 0 comments Cited 631 times – based on 0 reviews     Review now
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            Ocular changes in TgF344-AD rat model of Alzheimer's disease.

            Yuchun Tsai, Jia-Bin Lu, Alexander V. Ljubimov … (2014)
            Alzheimer's disease (AD) is the most common neurodegenerative disorder characterized by progressive decline in learning, memory, and executive functions. In addition to cognitive and behavioral deficits, vision disturbances have been reported in early stage of AD, well before the diagnosis is clearly established. To further investigate ocular abnormalities, a novel AD transgenic rat model was analyzed.
            Article 0 comments Cited 78 times – based on 0 reviews     Review now
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              Glucocerebrosidase deficiency accelerates the accumulation of proteinase K-resistant α-synuclein and aggravates neurodegeneration in a Drosophila model of Parkinson's disease.

              Mari Suzuki, Nobuhiro Fujikake, Toshihide Takeuchi … (2015)
              Alpha-synuclein (αSyn) plays a central role in the pathogenesis of Parkinson's disease (PD) and dementia with Lewy bodies (DLB). Recent multicenter genetic studies have revealed that mutations in the glucocerebrosidase 1 (GBA1) gene, which are responsible for Gaucher's disease, are strong risk factors for PD and DLB. However, the mechanistic link between the functional loss of glucocerebrosidase (GCase) and the toxicity of αSyn in vivo is not fully understood. In this study, we employed Drosophila models to examine the effect of GCase deficiency on the neurotoxicity of αSyn and its molecular mechanism. Behavioral and histological analyses showed that knockdown of the Drosophila homolog of GBA1 (dGBA1) exacerbates the locomotor dysfunction, loss of dopaminergic neurons and retinal degeneration of αSyn-expressing flies. This phenotypic aggravation was associated with the accumulation of proteinase K (PK)-resistant αSyn, rather than with changes in the total amount of αSyn, raising the possibility that glucosylceramide (GlcCer), a substrate of GCase, accelerates the misfolding of αSyn. Indeed, in vitro experiments revealed that GlcCer directly promotes the conversion of recombinant αSyn into the PK-resistant form, representing a toxic conformational change. Similar to dGBA1 knockdown, knockdown of the Drosophila homolog of β-galactosidase (β-Gal) also aggravated locomotor dysfunction of the αSyn flies, and its substrate GM1 ganglioside accelerated the formation of PK-resistant αSyn. Our findings suggest that the functional loss of GCase or β-Gal promotes the toxic conversion of αSyn via aberrant interactions between αSyn and their substrate glycolipids, leading to the aggravation of αSyn-mediated neurodegeneration.
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                Author and article information

                Contributors
                Tobias Lindner:
                ORCID: http://orcid.org/0000-0001-7826-3132
                tobias.lindner@med.uni-rostock.de
                Journal
                Journal ID (nlm-ta): Sci Rep
                Journal ID (iso-abbrev): Sci Rep
                Title: Scientific Reports
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2045-2322
                Publication date (Electronic): 1 June 2017
                Publication date PMC-release: 1 June 2017
                Publication date Collection: 2017
                Volume: 7
                Electronic Location Identifier: 2647
                Affiliations
                [1 ]ISNI 0000 0000 9737 0454, GRID grid.413108.f, Core Facility Multimodal Small Animal Imaging, , Rostock University Medical Center, ; Rostock, Germany
                [2 ]ISNI 0000 0000 9737 0454, GRID grid.413108.f, Department of Ophthalmology, , Rostock University Medical Center, ; Rostock, Germany
                [3 ]GRID grid.5603.0, Institute for Diagnostic Radiology and Neuroradiology, , University Medicine Greifswald, ; Greifswald, Germany
                [4 ]ISNI 0000 0000 9737 0454, GRID grid.413108.f, Institute of Anatomy, , Rostock University Medical Center, ; Rostock, Germany
                [5 ]ISNI 0000 0000 9737 0454, GRID grid.413108.f, Medical Biology and Electron Microscopy Centre, , Rostock University Medical Center, ; Rostock, Germany
                [6 ]ISNI 0000 0000 9737 0454, GRID grid.413108.f, Institute for Biostatistics and Informatics in Medicine and Ageing Research, , Rostock University Medical Center, ; Rostock, Germany
                [7 ]Institut und Poliklinik für Radiologische Diagnostik, Carl Gustav Carus University, Dresden, Germany
                Author information
                http://orcid.org/0000-0001-7826-3132
                http://orcid.org/0000-0001-5831-0608
                http://orcid.org/0000-0002-2517-4440
                Article
                Publisher ID: 2755
                DOI: 10.1038/s41598-017-02755-4
                PMC ID: 5453995
                PubMed ID: 28572591
                SO-VID: 56536c28-7cce-4a5c-ac79-4be96e472a89
                Copyright © © The Author(s) 2017
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 9 January 2017
                Date accepted : 18 April 2017
                Categories
                Subject: Article
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                issue-copyright-statement © The Author(s) 2017

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