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Article ; Online: Affordable optical clearing and immunolabelling in mouse brain slices.

Muza, Phillip M / Pérez, Marta / Noy, Suzanna / Kurosawa, Miyu / Katsouri, Loukia / Tybulewicz, Victor L J / Fisher, Elizabeth M C / West, Steven J

BMC research notes

2023 Volume 16, Issue 1, Page(s) 246

Abstract: Traditional histological analysis is conducted on thin tissue sections, limiting the data capture from large tissue volumes to 2D profiles, and requiring stereological methods for 3D assessment. Recent advances in microscopical and tissue clearing ... ...

Abstract	Traditional histological analysis is conducted on thin tissue sections, limiting the data capture from large tissue volumes to 2D profiles, and requiring stereological methods for 3D assessment. Recent advances in microscopical and tissue clearing methods have facilitated 3D reconstructions of tissue structure. However, staining of large tissue blocks remains a challenge, often requiring specialised and expensive equipment to clear and immunolabel tissue. Here, we present the Affordable Brain Slice Optical Clearing (ABSOC) method: a modified iDISCO protocol which enables clearing and immunolabeling of mouse brain slices up to 1 mm thick using inexpensive reagents and equipment, with no intensive expert training required. We illustrate the use of ABSOC in 1 mm C57BL/6J mouse coronal brain slices sectioned through the dorsal hippocampus and immunolabelled with an anti-calretinin antibody. The ABSOC method can be readily used for histological studies of mouse brain in order to move from the use of very thin tissue sections to large volumes of tissue - giving more representative analysis of biological samples, without the need for sampling of small regions only.
MeSH term(s)	Mice ; Animals ; Mice, Inbred C57BL ; Brain ; Microscopy/methods ; Imaging, Three-Dimensional/methods ; Specimen Handling
Language	English
Publishing date	2023-09-30
Publishing country	England
Document type	Journal Article
ZDB-ID	2413336-X
ISSN	1756-0500 ; 1756-0500
ISSN (online)	1756-0500
ISSN	1756-0500
DOI	10.1186/s13104-023-06511-y
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Article ; Online: Cathepsin B abundance, activity and microglial localisation in Alzheimer's disease-Down syndrome and early onset Alzheimer's disease; the role of elevated cystatin B.

Wu, Yixing / Mumford, Paige / Noy, Suzanna / Cleverley, Karen / Mrzyglod, Alicja / Luo, Dinghao / van Dalen, Floris / Verdoes, Martijn / Fisher, Elizabeth M C / Wiseman, Frances K

Acta neuropathologica communications

2023 Volume 11, Issue 1, Page(s) 132

Abstract: Cathepsin B is a cysteine protease that is implicated in multiple aspects of Alzheimer's disease pathogenesis. The endogenous inhibitor of this enzyme, cystatin B (CSTB) is encoded on chromosome 21. Thus, individuals who have Down syndrome, a genetic ... ...

Abstract	Cathepsin B is a cysteine protease that is implicated in multiple aspects of Alzheimer's disease pathogenesis. The endogenous inhibitor of this enzyme, cystatin B (CSTB) is encoded on chromosome 21. Thus, individuals who have Down syndrome, a genetic condition caused by having an additional copy of chromosome 21, have an extra copy of an endogenous inhibitor of the enzyme. Individuals who have Down syndrome are also at significantly increased risk of developing early-onset Alzheimer's disease (EOAD). The impact of the additional copy of CSTB on Alzheimer's disease development in people who have Down syndrome is not well understood. Here we compared the biology of cathepsin B and CSTB in individuals who had Down syndrome and Alzheimer's disease, with disomic individuals who had Alzheimer's disease or were ageing healthily. We find that the activity of cathepsin B enzyme is decreased in the brain of people who had Down syndrome and Alzheimer's disease compared with disomic individuals who had Alzheimer's disease. This change occurs independently of an alteration in the abundance of the mature enzyme or the number of cathepsin B
MeSH term(s)	Humans ; Mice ; Animals ; Down Syndrome/pathology ; Alzheimer Disease/pathology ; Cystatin B/genetics ; Cathepsin B ; Microglia/metabolism
Chemical Substances	Cystatin B (88844-95-5) ; Cathepsin B (EC 3.4.22.1)
Language	English
Publishing date	2023-08-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2715589-4
ISSN	2051-5960 ; 2051-5960
ISSN (online)	2051-5960
ISSN	2051-5960
DOI	10.1186/s40478-023-01632-8
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Article ; Online: The effects of Cstb duplication on APP/amyloid-β pathology and cathepsin B activity in a mouse model.

Wu, Yixing / Whittaker, Heather T / Noy, Suzanna / Cleverley, Karen / Brault, Veronique / Herault, Yann / Fisher, Elizabeth M C / Wiseman, Frances K

PloS one

2021 Volume 16, Issue 7, Page(s) e0242236

Abstract: People with Down syndrome (DS), caused by trisomy of chromosome 21 have a greatly increased risk of developing Alzheimer's disease (AD). This is in part because of triplication of a chromosome 21 gene, APP. This gene encodes amyloid precursor protein, ... ...

Abstract	People with Down syndrome (DS), caused by trisomy of chromosome 21 have a greatly increased risk of developing Alzheimer's disease (AD). This is in part because of triplication of a chromosome 21 gene, APP. This gene encodes amyloid precursor protein, which is cleaved to form amyloid-β that accumulates in the brains of people who have AD. Recent experimental results demonstrate that a gene or genes on chromosome 21, other than APP, when triplicated significantly accelerate amyloid-β pathology in a transgenic mouse model of amyloid-β deposition. Multiple lines of evidence indicate that cysteine cathepsin activity influences APP cleavage and amyloid-β accumulation. Located on human chromosome 21 (Hsa21) is an endogenous inhibitor of cathepsin proteases, CYSTATIN B (CSTB) which is proposed to regulate cysteine cathepsin activity in vivo. Here we determined if three copies of the mouse gene Cstb is sufficient to modulate amyloid-β accumulation and cathepsin activity in a transgenic APP mouse model. Duplication of Cstb resulted in an increase in transcriptional and translational levels of Cstb in the mouse cortex but had no effect on the deposition of insoluble amyloid-β plaques or the levels of soluble or insoluble amyloid-β42, amyloid-β40, or amyloid-β38 in 6-month old mice. In addition, the increased CSTB did not alter the activity of cathepsin B enzyme in the cortex of 3-month or 6-month old mice. These results indicate that the single-gene duplication of Cstb is insufficient to elicit a disease-modifying phenotype in the dupCstb x tgAPP mice, underscoring the complexity of the genetic basis of AD-DS and the importance of multiple gene interactions in disease.
MeSH term(s)	Aging ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Amyloid beta-Peptides/genetics ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/genetics ; Amyloid beta-Protein Precursor/metabolism ; Animals ; Cathepsin B/metabolism ; Cerebral Cortex/enzymology ; Cerebral Cortex/metabolism ; Cystatin B/genetics ; Cystatin B/metabolism ; Disease Models, Animal ; Female ; Gene Duplication ; Hippocampus/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic
Chemical Substances	Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; Cystatin B (88844-95-5) ; Cathepsin B (EC 3.4.22.1)
Language	English
Publishing date	2021-07-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0242236
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Article ; Online: Altered Hippocampal-Prefrontal Neural Dynamics in Mouse Models of Down Syndrome.

Chang, Pishan / Bush, Daniel / Schorge, Stephanie / Good, Mark / Canonica, Tara / Shing, Nathanael / Noy, Suzanna / Wiseman, Frances K / Burgess, Neil / Tybulewicz, Victor L J / Walker, Matthew C / Fisher, Elizabeth M C

Cell reports

2020 Volume 30, Issue 4, Page(s) 1152–1163.e4

Abstract: Altered neural dynamics in the medial prefrontal cortex (mPFC) and hippocampus may contribute to cognitive impairments in the complex chromosomal disorder Down syndrome (DS). Here, we demonstrate non-overlapping behavioral differences associated with ... ...

Abstract	Altered neural dynamics in the medial prefrontal cortex (mPFC) and hippocampus may contribute to cognitive impairments in the complex chromosomal disorder Down syndrome (DS). Here, we demonstrate non-overlapping behavioral differences associated with distinct abnormalities in hippocampal and mPFC electrophysiology during a canonical spatial working memory task in three partially trisomic mouse models of DS (Dp1Tyb, Dp10Yey, and Dp17Yey) that together cover all regions of homology with human chromosome 21 (Hsa21). Dp1Tyb mice show slower decision-making (unrelated to the gene dose of DYRK1A, which has been implicated in DS cognitive dysfunction) and altered theta dynamics (reduced frequency, increased hippocampal-mPFC coherence, and increased modulation of hippocampal high gamma); Dp10Yey mice show impaired alternation performance and reduced theta modulation of hippocampal low gamma; and Dp17Yey mice are not significantly different from the wild type. These results link specific hippocampal and mPFC circuit dysfunctions to cognitive deficits in DS models and, importantly, map them to discrete regions of Hsa21.
MeSH term(s)	Animals ; Chromosomes, Human, Pair 21/genetics ; Cognitive Dysfunction/genetics ; Cognitive Dysfunction/physiopathology ; Disease Models, Animal ; Down Syndrome/genetics ; Electroencephalography ; Hippocampus/metabolism ; Hippocampus/physiopathology ; Humans ; Male ; Memory, Short-Term/physiology ; Mice ; Mice, Inbred C57BL ; Prefrontal Cortex/metabolism ; Prefrontal Cortex/physiology ; Protein Serine-Threonine Kinases/genetics ; Protein Serine-Threonine Kinases/metabolism ; Protein-Tyrosine Kinases/genetics ; Protein-Tyrosine Kinases/metabolism ; Spatial Memory/physiology ; Theta Rhythm/genetics ; Trisomy/genetics ; Trisomy/physiopathology ; Dyrk Kinases
Chemical Substances	Protein-Tyrosine Kinases (EC 2.7.10.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2020-01-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2019.12.065
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Article ; Online: CNS elevation of vascular and not mucosal addressin cell adhesion molecules in patients with multiple sclerosis.

Allavena, Rachel / Noy, Suzanna / Andrews, Marcus / Pullen, Nick

The American journal of pathology

2009 Volume 176, Issue 2, Page(s) 556–562

Abstract: The mucosal addressin cell adhesion molecule (MAdCAM) and vascular cell adhesion molecule (VCAM) appear to play roles in the recruitment of leukocytes to specialized endothelium lining the gastrointestinal tract. The purpose of this study was to clarify ... ...

Abstract	The mucosal addressin cell adhesion molecule (MAdCAM) and vascular cell adhesion molecule (VCAM) appear to play roles in the recruitment of leukocytes to specialized endothelium lining the gastrointestinal tract. The purpose of this study was to clarify the role of MAdCAM and VCAM in the central nervous system by comparing protein expression in patients with multiple sclerosis (MS) and control subjects by immunohistochemistry. Specific antibodies to human VCAM and MAdCAM were used to confirm expression in control and MS nervous system specimens by immunohistochemistry. VCAM immunoreactivity was detected in endothelial cells, perivascular tissue, and in some cases, leukocytes within the meninges, gray, and white matter, of both controls and MS patients. VCAM immunoreactivity was maximal in a patient with acute active plaques, but of lower intensity and reduced distribution in controls and those with chronic active or inactive MS plaques. In contrast, MAdCAM immunoreactivity could not be detected in brain tissue from unaffected or MS patients. Taken together, these data support a role of VCAM, but not MAdCAM in the development of MS.
MeSH term(s)	Case-Control Studies ; Cell Adhesion Molecules ; Central Nervous System/metabolism ; Central Nervous System/pathology ; Female ; Humans ; Ileum/metabolism ; Ileum/pathology ; Immunoglobulins/metabolism ; Immunohistochemistry ; Male ; Mucoproteins/metabolism ; Multiple Sclerosis/metabolism ; Multiple Sclerosis/pathology ; Plaque, Amyloid/metabolism ; Plaque, Amyloid/pathology ; Up-Regulation ; Vascular Cell Adhesion Molecule-1/metabolism
Chemical Substances	Cell Adhesion Molecules ; Immunoglobulins ; MADCAM1 protein, human ; Mucoproteins ; Vascular Cell Adhesion Molecule-1
Language	English
Publishing date	2009-12-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.2353/ajpath.2010.090437
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Article ; Online: T

Whittaker, Heather T / Zhu, Shenghua / Di Curzio, Domenico L / Buist, Richard / Li, Xin-Min / Noy, Suzanna / Wiseman, Frances K / Thiessen, Jonathan D / Martin, Melanie

Magnetic resonance imaging

2018 Volume 50, Page(s) 26–37

Abstract: Alzheimer's disease (AD) pathology causes microstructural changes in the brain. These changes, if quantified with magnetic resonance imaging (MRI), could be studied for use as an early biomarker for AD. The aim of our study was to determine if ... ...

Abstract	Alzheimer's disease (AD) pathology causes microstructural changes in the brain. These changes, if quantified with magnetic resonance imaging (MRI), could be studied for use as an early biomarker for AD. The aim of our study was to determine if T
MeSH term(s)	Alzheimer Disease/diagnostic imaging ; Alzheimer Disease/pathology ; Animals ; Diffusion Magnetic Resonance Imaging/methods ; Diffusion Tensor Imaging/methods ; Disease Models, Animal ; Hippocampus/diagnostic imaging ; Hippocampus/pathology ; Humans ; Image Processing, Computer-Assisted/methods ; Male ; Mice ; Mice, Transgenic
Language	English
Publishing date	2018-03-12
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604885-7
ISSN	1873-5894 ; 0730-725X
ISSN (online)	1873-5894
ISSN	0730-725X
DOI	10.1016/j.mri.2018.03.010
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Article ; Online: Comprehensive phenotypic analysis of the Dp1Tyb mouse strain reveals a broad range of Down syndrome-related phenotypes.

Lana-Elola, Eva / Cater, Heather / Watson-Scales, Sheona / Greenaway, Simon / Müller-Winkler, Jennifer / Gibbins, Dorota / Nemes, Mihaela / Slender, Amy / Hough, Tertius / Keskivali-Bond, Piia / Scudamore, Cheryl L / Herbert, Eleanor / Banks, Gareth T / Mobbs, Helene / Canonica, Tara / Tosh, Justin / Noy, Suzanna / Llorian, Miriam / Nolan, Patrick M /

Griffin, Julian L / Good, Mark / Simon, Michelle / Mallon, Ann-Marie / Wells, Sara / Fisher, Elizabeth M C / Tybulewicz, Victor L J

Disease models & mechanisms

2021 Volume 14, Issue 10

Abstract: Down syndrome (DS), trisomy 21, results in many complex phenotypes including cognitive deficits, heart defects and craniofacial alterations. Phenotypes arise from an extra copy of human chromosome 21 (Hsa21) genes. However, these dosage-sensitive ... ...

Abstract	Down syndrome (DS), trisomy 21, results in many complex phenotypes including cognitive deficits, heart defects and craniofacial alterations. Phenotypes arise from an extra copy of human chromosome 21 (Hsa21) genes. However, these dosage-sensitive causative genes remain unknown. Animal models enable identification of genes and pathological mechanisms. The Dp1Tyb mouse model of DS has an extra copy of 63% of Hsa21-orthologous mouse genes. In order to establish whether this model recapitulates DS phenotypes, we comprehensively phenotyped Dp1Tyb mice using 28 tests of different physiological systems and found that 468 out of 1800 parameters were significantly altered. We show that Dp1Tyb mice have wide-ranging DS-like phenotypes, including aberrant erythropoiesis and megakaryopoiesis, reduced bone density, craniofacial changes, altered cardiac function, a pre-diabetic state, and deficits in memory, locomotion, hearing and sleep. Thus, Dp1Tyb mice are an excellent model for investigating complex DS phenotype-genotype relationships for this common disorder.
MeSH term(s)	Amyloid beta-Peptides/metabolism ; Anemia/complications ; Animals ; Bone Development ; Disease Models, Animal ; Down Syndrome/genetics ; Down Syndrome/pathology ; Down Syndrome/physiopathology ; Erythropoiesis ; Evoked Potentials, Auditory, Brain Stem ; Gene Expression Regulation ; Genes, Duplicate ; Hearing ; Heart Function Tests ; Hippocampus/pathology ; Locomotion ; Memory/physiology ; Mice, Inbred C57BL ; Otitis Media/complications ; Otitis Media/pathology ; Otitis Media/physiopathology ; Phenotype ; Prediabetic State/complications ; Prediabetic State/pathology ; Prediabetic State/physiopathology ; Respiration ; Sleep/physiology ; Spleen/pathology ; Splenomegaly/complications ; Mice
Chemical Substances	Amyloid beta-Peptides
Language	English
Publishing date	2021-10-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2451104-3
ISSN	1754-8411 ; 1754-8403
ISSN (online)	1754-8411
ISSN	1754-8403
DOI	10.1242/dmm.049157
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Article ; Online: Humanized mutant FUS drives progressive motor neuron degeneration without aggregation in 'FUSDelta14' knockin mice.

Brain : a journal of neurology

2017 Volume 140, Issue 11, Page(s) 2797–2805

Abstract: Mutations in FUS are causative for amyotrophic lateral sclerosis with a dominant mode of inheritance. In trying to model FUS-amyotrophic lateral sclerosis (ALS) in mouse it is clear that FUS is dosage-sensitive and effects arise from overexpression per ... ...

Abstract	Mutations in FUS are causative for amyotrophic lateral sclerosis with a dominant mode of inheritance. In trying to model FUS-amyotrophic lateral sclerosis (ALS) in mouse it is clear that FUS is dosage-sensitive and effects arise from overexpression per se in transgenic strains. Novel models are required that maintain physiological levels of FUS expression and that recapitulate the human disease-with progressive loss of motor neurons in heterozygous animals. Here, we describe a new humanized FUS-ALS mouse with a frameshift mutation, which fulfils both criteria: the FUS Delta14 mouse. Heterozygous animals express mutant humanized FUS protein at physiological levels and have adult onset progressive motor neuron loss and denervation of neuromuscular junctions. Additionally, we generated a novel antibody to the unique human frameshift peptide epitope, allowing specific identification of mutant FUS only. Using our new FUSDelta14 ALS mouse-antibody system we show that neurodegeneration occurs in the absence of FUS protein aggregation. FUS mislocalization increases as disease progresses, and mutant FUS accumulates at the rough endoplasmic reticulum. Further, transcriptomic analyses show progressive changes in ribosomal protein levels and mitochondrial function as early disease stages are initiated. Thus, our new physiological mouse model has provided novel insight into the early pathogenesis of FUS-ALS.
MeSH term(s)	Amyotrophic Lateral Sclerosis/genetics ; Amyotrophic Lateral Sclerosis/metabolism ; Animals ; Disease Models, Animal ; Endoplasmic Reticulum, Rough/metabolism ; Frameshift Mutation ; Gene Dosage ; Gene Expression Profiling ; Gene Knock-In Techniques ; Heterozygote ; Humans ; Mice ; Mitochondria/metabolism ; Motor Neurons/metabolism ; Neuromuscular Junction/metabolism ; Protein Aggregation, Pathological/genetics ; Protein Aggregation, Pathological/metabolism ; RNA-Binding Protein FUS/genetics ; RNA-Binding Protein FUS/metabolism ; Ribosomal Proteins/genetics
Chemical Substances	RNA-Binding Protein FUS ; Ribosomal Proteins
Language	English
Publishing date	2017-10-18
Publishing country	England
Document type	Journal Article
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awx248
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Article ; Online: Affordable optical clearing and immunolabelling in mouse brain slices.

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Article ; Online: Cathepsin B abundance, activity and microglial localisation in Alzheimer's disease-Down syndrome and early onset Alzheimer's disease; the role of elevated cystatin B.

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Article ; Online: The effects of Cstb duplication on APP/amyloid-β pathology and cathepsin B activity in a mouse model.

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Article ; Online: Altered Hippocampal-Prefrontal Neural Dynamics in Mouse Models of Down Syndrome.

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Article ; Online: CNS elevation of vascular and not mucosal addressin cell adhesion molecules in patients with multiple sclerosis.

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Article ; Online: T

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Article ; Online: Comprehensive phenotypic analysis of the Dp1Tyb mouse strain reveals a broad range of Down syndrome-related phenotypes.

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Article ; Online: Humanized mutant FUS drives progressive motor neuron degeneration without aggregation in 'FUSDelta14' knockin mice.

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