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Article ; Online: Trisomy of Human Chromosome 21 Orthologs Mapping to Mouse Chromosome 10 Cause Age and Sex-Specific Learning Differences: Relevance to Down Syndrome.

Minter, Ross / Gardiner, Katheleen J

2021 Volume 12, Issue 11

Abstract: Down syndrome (DS), trisomy of human chromosome 21 (Hsa21), is the most common genetic cause of intellectual disability. The Dp10(1)Yey (Dp10) is a mouse model of DS that is trisomic for orthologs of 25% of the Hsa21 protein-coding genes, the entirety of ...

Abstract	Down syndrome (DS), trisomy of human chromosome 21 (Hsa21), is the most common genetic cause of intellectual disability. The Dp10(1)Yey (Dp10) is a mouse model of DS that is trisomic for orthologs of 25% of the Hsa21 protein-coding genes, the entirety of the Hsa21 syntenic region on mouse chromosome 10. Trisomic genes include several involved in brain development and function, two that modify and regulate the activities of sex hormones, and two that produce sex-specific phenotypes as null mutants. These last four are the only Hsa21 genes with known sexually dimorphic properties. Relatively little is known about the potential contributions to the DS phenotype of segmental trisomy of Mmu10 orthologs. Here, we have tested separate cohorts of female and male Dp10 mice, at 3 and 9 months of age, in an open field elevated zero maze, rotarod, and balance beam, plus the learning and memory tasks, spontaneous alternation, puzzle box, double-H maze, context fear conditioning, and acoustic startle/prepulse inhibition, that depend upon the function of the prefrontal cortex, striatum, hippocampus, and cerebellum. We show that there are age and sex-specific differences in strengths and weaknesses, suggesting that genes within the telomere proximal region of Hsa21 influence the DS phenotype.
MeSH term(s)	Age Factors ; Animals ; Behavior, Animal ; Chromosome Mapping ; Chromosomes, Mammalian/genetics ; Disease Models, Animal ; Down Syndrome/genetics ; Down Syndrome/pathology ; Female ; Humans ; Learning/physiology ; Male ; Maze Learning/physiology ; Mice/genetics ; Mice, Inbred C57BL ; Phenotype ; Sex Characteristics
Language	English
Publishing date	2021-10-26
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2527218-4
ISSN	2073-4425 ; 2073-4425
ISSN (online)	2073-4425
ISSN	2073-4425
DOI	10.3390/genes12111697
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Article: Trisomy of Human Chromosome 21 Orthologs Mapping to Mouse Chromosome 10 Cause Age and Sex-Specific Learning Differences: Relevance to Down Syndrome

Minter, Ross / Gardiner, Katheleen J.

Genes. 2021 Oct. 26, v. 12, no. 11

2021

Abstract	Down syndrome (DS), trisomy of human chromosome 21 (Hsa21), is the most common genetic cause of intellectual disability. The Dp10(1)Yey (Dp10) is a mouse model of DS that is trisomic for orthologs of 25% of the Hsa21 protein-coding genes, the entirety of the Hsa21 syntenic region on mouse chromosome 10. Trisomic genes include several involved in brain development and function, two that modify and regulate the activities of sex hormones, and two that produce sex-specific phenotypes as null mutants. These last four are the only Hsa21 genes with known sexually dimorphic properties. Relatively little is known about the potential contributions to the DS phenotype of segmental trisomy of Mmu10 orthologs. Here, we have tested separate cohorts of female and male Dp10 mice, at 3 and 9 months of age, in an open field elevated zero maze, rotarod, and balance beam, plus the learning and memory tasks, spontaneous alternation, puzzle box, double-H maze, context fear conditioning, and acoustic startle/prepulse inhibition, that depend upon the function of the prefrontal cortex, striatum, hippocampus, and cerebellum. We show that there are age and sex-specific differences in strengths and weaknesses, suggesting that genes within the telomere proximal region of Hsa21 influence the DS phenotype.
Keywords	Down syndrome ; acoustics ; cerebellum ; fearfulness ; females ; hippocampus ; humans ; males ; memory ; mice ; phenotype ; prefrontal cortex ; sexual dimorphism ; telomeres ; trisomics
Language	English
Dates of publication	2021-1026
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2527218-4
ISSN	2073-4425
ISSN	2073-4425
DOI	10.3390/genes12111697
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Article ; Online: Pharmacological approaches to improving cognitive function in Down syndrome: current status and considerations.

Gardiner, Katheleen J

Drug design, development and therapy

2015 Volume 9, Page(s) 103–125

Abstract: Down syndrome (DS), also known as trisomy 21, is the most common genetic cause of intellectual disability (ID). Although ID can be mild, the average intelligence quotient is in the range of 40-50. All individuals with DS will also develop the ... ...

Abstract	Down syndrome (DS), also known as trisomy 21, is the most common genetic cause of intellectual disability (ID). Although ID can be mild, the average intelligence quotient is in the range of 40-50. All individuals with DS will also develop the neuropathology of Alzheimer's disease (AD) by the age of 30-40 years, and approximately half will display an AD-like dementia by the age of 60 years. DS is caused by an extra copy of the long arm of human chromosome 21 (Hsa21) and the consequent elevated levels of expression, due to dosage, of trisomic genes. Despite a worldwide incidence of one in 700-1,000 live births, there are currently no pharmacological treatments available for ID or AD in DS. However, over the last several years, very promising results have been obtained with a mouse model of DS, the Ts65Dn. A diverse array of drugs has been shown to rescue, or partially rescue, DS-relevant deficits in learning and memory and abnormalities in cellular and electrophysiological features seen in the Ts65Dn. These results suggest that some level of amelioration or prevention of cognitive deficits in people with DS may be possible. Here, we review information from the preclinical evaluations in the Ts65Dn, how drugs were selected, how efficacy was judged, and how outcomes differ, or not, among studies. We also summarize the current state of human clinical trials for ID and AD in DS. Lastly, we describe the genetic limitations of the Ts65Dn as a model of DS, and in the preclinical testing of pharmacotherapeutics, and suggest additional targets to be considered for potential pharmacotherapies.
MeSH term(s)	Animals ; Cognition Disorders/drug therapy ; Cognition Disorders/genetics ; Down Syndrome/drug therapy ; Down Syndrome/genetics ; Humans ; Neuroprotective Agents/therapeutic use
Chemical Substances	Neuroprotective Agents
Language	English
Publishing date	2015
Publishing country	New Zealand
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2451346-5
ISSN	1177-8881 ; 1177-8881
ISSN (online)	1177-8881
ISSN	1177-8881
DOI	10.2147/DDDT.S51476
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Article: All Creatures Great and Small: New Approaches for Understanding Down Syndrome Genetics.

Moyer, Anna J / Gardiner, Katheleen / Reeves, Roger H

Trends in genetics : TIG

2020 Volume 37, Issue 5, Page(s) 444–459

Abstract: Human chromosome 21 (Hsa21) contains more than 500 genes, making trisomy 21 one of the most complex genetic perturbations compatible with life. The ultimate goal of Down syndrome (DS) research is to design therapies that improve quality of life for ... ...

Abstract	Human chromosome 21 (Hsa21) contains more than 500 genes, making trisomy 21 one of the most complex genetic perturbations compatible with life. The ultimate goal of Down syndrome (DS) research is to design therapies that improve quality of life for individuals with DS by understanding which subsets of Hsa21 genes contribute to DS-associated phenotypes throughout the lifetime. However, the complexity of DS pathogenesis has made developing appropriate animal models an ongoing challenge. Here, we examine lessons learned from a variety of model systems, including yeast, nematode, fruit fly, and zebrafish, and discuss emerging methods for creating murine models that better reflect the genetic basis of trisomy 21.
MeSH term(s)	Aneuploidy ; Animals ; Chromosomes, Human, Pair 21/genetics ; Disease Models, Animal ; Down Syndrome/genetics ; Drosophila/genetics ; Genomics/methods ; Humans ; Mice ; Pan troglodytes/genetics ; Rats ; Yeasts/genetics ; Zebrafish/genetics
Language	English
Publishing date	2020-10-20
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	619240-3
ISSN	1362-4555 ; 0168-9525 ; 0168-9479
ISSN (online)	1362-4555
ISSN	0168-9525 ; 0168-9479
DOI	10.1016/j.tig.2020.09.017
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Article ; Online: Context Fear Conditioning in Down Syndrome Mouse Models: Effects of Trisomic Gene Content, Age, Sex and Genetic Background.

Ahmed, Md Mahiuddin / Block, Aaron / Busquet, Nicolas / Gardiner, Katheleen J

Genes

2021 Volume 12, Issue 10

Abstract: Down syndrome (DS), trisomy of the long arm of human chromosome 21 (Hsa21), is the most common genetic cause of intellectual disability (ID). Currently, there are no effective pharmacotherapies. The success of clinical trials to improve cognition depends ...

Abstract	Down syndrome (DS), trisomy of the long arm of human chromosome 21 (Hsa21), is the most common genetic cause of intellectual disability (ID). Currently, there are no effective pharmacotherapies. The success of clinical trials to improve cognition depends in part on the design of preclinical evaluations in mouse models. To broaden understanding of the common limitations of experiments in learning and memory, we report performance in context fear conditioning (CFC) in three mouse models of DS, the Dp(16)1Yey, Dp(17)1Yey and Dp(10)1Yey (abbreviated Dp16, Dp17 and Dp10), separately trisomic for the human Hsa21 orthologs mapping to mouse chromosomes 16, 17 and 10, respectively. We examined female and male mice of the three lines on the standard C57BL/6J background at 3 months of age and Dp17 and Dp10 at 18 months of age. We also examined female and male mice of Dp17 and Dp10 at 3 months of age as F1 hybrids obtained from a cross with the DBA/2J background. Results indicate that genotype, sex, age and genetic background affect CFC performance. These data support the need to use both female and male mice, trisomy of sets of all Hsa21 orthologs, and additional ages and genetic backgrounds to improve the reliability of preclinical evaluations of drugs for ID in DS.
MeSH term(s)	Animals ; Conditioning, Classical ; Down Syndrome/genetics ; Down Syndrome/physiopathology ; Fear ; Female ; Genetic Background ; Hippocampus/growth & development ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Sex Characteristics
Language	English
Publishing date	2021-09-28
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2527218-4
ISSN	2073-4425 ; 2073-4425
ISSN (online)	2073-4425
ISSN	2073-4425
DOI	10.3390/genes12101528
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Article: Context Fear Conditioning in Down Syndrome Mouse Models: Effects of Trisomic Gene Content, Age, Sex and Genetic Background

Ahmed, Md. Mahiuddin / Block, Aaron / Busquet, Nicolas / Gardiner, Katheleen J.

Genes. 2021 Sept. 28, v. 12, no. 10

2021

Abstract	Down syndrome (DS), trisomy of the long arm of human chromosome 21 (Hsa21), is the most common genetic cause of intellectual disability (ID). Currently, there are no effective pharmacotherapies. The success of clinical trials to improve cognition depends in part on the design of preclinical evaluations in mouse models. To broaden understanding of the common limitations of experiments in learning and memory, we report performance in context fear conditioning (CFC) in three mouse models of DS, the Dp(16)1Yey, Dp(17)1Yey and Dp(10)1Yey (abbreviated Dp16, Dp17 and Dp10), separately trisomic for the human Hsa21 orthologs mapping to mouse chromosomes 16, 17 and 10, respectively. We examined female and male mice of the three lines on the standard C57BL/6J background at 3 months of age and Dp17 and Dp10 at 18 months of age. We also examined female and male mice of Dp17 and Dp10 at 3 months of age as F1 hybrids obtained from a cross with the DBA/2J background. Results indicate that genotype, sex, age and genetic background affect CFC performance. These data support the need to use both female and male mice, trisomy of sets of all Hsa21 orthologs, and additional ages and genetic backgrounds to improve the reliability of preclinical evaluations of drugs for ID in DS.
Keywords	Down syndrome ; chromosomes ; cognition ; drug therapy ; fearfulness ; females ; genes ; genetic background ; humans ; males ; memory ; mice ; trisomics
Language	English
Dates of publication	2021-0928
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2527218-4
ISSN	2073-4425
ISSN	2073-4425
DOI	10.3390/genes12101528
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Article ; Online: RPPAware: A software suite to preprocess, analyze and visualize reverse phase protein array data.

Ranjitha Dhanasekaran, A / Gardiner, Katheleen J

Journal of bioinformatics and computational biology

2018 Volume 16, Issue 3, Page(s) 1850001

Abstract: Reverse Phase Protein Arrays (RPPA) is a high-throughput technology used to profile levels of protein expression. Handling the large datasets generated by RPPA can be facilitated by appropriate software tools. Here, we describe RPPAware, a free and ... ...

Abstract	Reverse Phase Protein Arrays (RPPA) is a high-throughput technology used to profile levels of protein expression. Handling the large datasets generated by RPPA can be facilitated by appropriate software tools. Here, we describe RPPAware, a free and intuitive software suite that was developed specifically for analysis and visualization of RPPA data. RPPAware is a portable tool that requires no installation and was built using Java. Many modules of the tool invoke R to utilize the statistical features. To demonstrate the utility of RPPAware, data generated from screening brain regions of a mouse model of Down syndrome with 62 antibodies were used as a case study. The ease of use and efficiency of RPPAware can accelerate data analysis to facilitate biological discovery. RPPAware 1.0 is freely available under GNU General Public License from the project website at http://downsyndrome.ucdenver.edu/iddrc/rppaware/home.htm along with a full documentation of the tool.
MeSH term(s)	Animals ; Antibodies/analysis ; Brain/metabolism ; Brain-Derived Neurotrophic Factor/metabolism ; Chromosomes, Human, Pair 21 ; Disease Models, Animal ; Down Syndrome/metabolism ; Humans ; Mice ; Protein Array Analysis/methods ; Protein Array Analysis/statistics & numerical data ; Protein Serine-Threonine Kinases/metabolism ; Protein-Tyrosine Kinases/metabolism ; Proto-Oncogene Proteins B-raf/metabolism ; Software ; User-Computer Interface ; bcl-Associated Death Protein/metabolism ; Dyrk Kinases
Chemical Substances	Antibodies ; Bad protein, mouse ; Bdnf protein, mouse ; Brain-Derived Neurotrophic Factor ; bcl-Associated Death Protein ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; Braf protein, mouse (EC 2.7.11.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1)
Language	English
Publishing date	2018-01-15
Publishing country	Singapore
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2115015-1
ISSN	1757-6334 ; 0219-7200
ISSN (online)	1757-6334
ISSN	0219-7200
DOI	10.1142/S0219720018500014
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Article ; Online: Molecular basis of pharmacotherapies for cognition in Down syndrome.

Gardiner, Katheleen J

Trends in pharmacological sciences

2009 Volume 31, Issue 2, Page(s) 66–73

Abstract: Intellectual disability in Down syndrome (DS) ranges from low normal to severely impaired and has a significant impact on the quality-of-life of the individuals affected and their families. Because the incidence of DS remains at approximately 1 in 700 ... ...

Abstract	Intellectual disability in Down syndrome (DS) ranges from low normal to severely impaired and has a significant impact on the quality-of-life of the individuals affected and their families. Because the incidence of DS remains at approximately 1 in 700 live births and the lifespan is now >50 years, development of pharmacotherapies for cognitive deficits is an important goal. DS is due to an extra copy of human chromosome 21 and has often been considered too complex a genetic abnormality to be amenable to intervention. However, recent successes in rescuing learning/memory impairments in a mouse model of DS suggest that this negative outlook may not be justified. In this contribution, we first review the DS phenotype, chromosome 21 gene content and mouse models. We then discuss recent successes and the remaining challenges in the identification of targets for and preclinical evaluation of potential therapeutics.
MeSH term(s)	Animals ; CD24 Antigen/genetics ; Cognition Disorders/drug therapy ; Disease Models, Animal ; Down Syndrome/psychology ; Humans ; Mice ; Oxidative Stress ; Phenotype ; Receptor, Serotonin, 5-HT1A/physiology ; Receptors, N-Methyl-D-Aspartate/physiology
Chemical Substances	CD24 Antigen ; Cd24a protein, mouse ; Receptors, N-Methyl-D-Aspartate ; Receptor, Serotonin, 5-HT1A (112692-38-3)
Language	English
Publishing date	2009-12-04
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	282846-7
ISSN	1873-3735 ; 0165-6147
ISSN (online)	1873-3735
ISSN	0165-6147
DOI	10.1016/j.tips.2009.10.010
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Zs.A 1513: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: The innate immune system stimulating cytokine GM-CSF improves learning/memory and interneuron and astrocyte brain pathology in Dp16 Down syndrome mice and improves learning/memory in wild-type mice.

Ahmed, Md Mahiuddin / Wang, Athena Ching-Jung / Elos, Mihret / Chial, Heidi J / Sillau, Stefan / Solano, D Adriana / Coughlan, Christina / Aghili, Leila / Anton, Paige / Markham, Neil / Adame, Vanesa / Gardiner, Katheleen J / Boyd, Timothy D / Potter, Huntington

Neurobiology of disease

2022 Volume 168, Page(s) 105694

Abstract: Down syndrome (DS) is characterized by chronic neuroinflammation, peripheral inflammation, astrogliosis, imbalanced excitatory/inhibitory neuronal function, and cognitive deficits in both humans and mouse models. Suppression of inflammation has been ... ...

Abstract	Down syndrome (DS) is characterized by chronic neuroinflammation, peripheral inflammation, astrogliosis, imbalanced excitatory/inhibitory neuronal function, and cognitive deficits in both humans and mouse models. Suppression of inflammation has been proposed as a therapeutic approach to treating DS co-morbidities, including intellectual disability (DS/ID). Conversely, we discovered previously that treatment with the innate immune system stimulating cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF), which has both pro- and anti-inflammatory activities, improved cognition and reduced brain pathology in a mouse model of Alzheimer's disease (AD), another inflammatory disorder, and improved cognition and reduced biomarkers of brain pathology in a phase II trial of humans with mild-to-moderate AD. To investigate the effects of GM-CSF treatment on DS/ID in the absence of AD, we assessed behavior and brain pathology in 12-14 month-old DS mice (Dp[16]1Yey) and their wild-type (WT) littermates, neither of which develop amyloid, and found that subcutaneous GM-CSF treatment (5 μg/day, five days/week, for five weeks) improved performance in the radial arm water maze in both Dp16 and WT mice compared to placebo. Dp16 mice also showed abnormal astrocyte morphology, increased percent area of GFAP staining in the hippocampus, clustering of astrocytes in the hippocampus, and reduced numbers of calretinin-positive interneurons in the entorhinal cortex and subiculum, and all of these brain pathologies were improved by GM-CSF treatment. These findings suggest that stimulating and/or modulating inflammation and the innate immune system with GM-CSF treatment may enhance cognition in both people with DS/ID and in the typical aging population.
MeSH term(s)	Aged ; Alzheimer Disease/drug therapy ; Alzheimer Disease/pathology ; Animals ; Astrocytes/metabolism ; Cognition ; Cytokines/metabolism ; Disease Models, Animal ; Down Syndrome/drug therapy ; Down Syndrome/pathology ; Granulocyte-Macrophage Colony-Stimulating Factor/metabolism ; Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology ; Hippocampus/metabolism ; Humans ; Immune System/metabolism ; Immune System/pathology ; Inflammation/drug therapy ; Inflammation/pathology ; Interneurons/metabolism ; Mice
Chemical Substances	Cytokines ; Granulocyte-Macrophage Colony-Stimulating Factor (83869-56-1)
Language	English
Publishing date	2022-03-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2022.105694
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Article ; Online: Mouse models of Down syndrome: gene content and consequences.

Gupta, Meenal / Dhanasekaran, A Ranjitha / Gardiner, Katheleen J

Mammalian genome : official journal of the International Mammalian Genome Society

2016 Volume 27, Issue 11-12, Page(s) 538–555

Abstract: Down syndrome (DS), trisomy of human chromosome 21 (Hsa21), is challenging to model in mice. Not only is it a contiguous gene syndrome spanning 35 Mb of the long arm of Hsa21, but orthologs of Hsa21 genes map to segments of three mouse chromosomes, Mmu16, ...

Abstract	Down syndrome (DS), trisomy of human chromosome 21 (Hsa21), is challenging to model in mice. Not only is it a contiguous gene syndrome spanning 35 Mb of the long arm of Hsa21, but orthologs of Hsa21 genes map to segments of three mouse chromosomes, Mmu16, Mmu17, and Mmu10. The Ts65Dn was the first viable segmental trisomy mouse model for DS; it is a partial trisomy currently popular in preclinical evaluations of drugs for cognition in DS. Limitations of the Ts65Dn are as follows: (i) it is trisomic for 125 human protein-coding orthologs, but only 90 of these are Hsa21 orthologs and (ii) it lacks trisomy for ~75 Hsa21 orthologs. In recent years, several additional mouse models of DS have been generated, each trisomic for a different subset of Hsa21 genes or their orthologs. To best exploit these models and interpret the results obtained with them, prior to proposing clinical trials, an understanding of their trisomic gene content, relative to full trisomy 21, is necessary. Here we first review the functional information on Hsa21 protein-coding genes and the more recent annotation of a large number of functional RNA genes. We then discuss the conservation and genomic distribution of Hsa21 orthologs in the mouse genome and the distribution of mouse-specific genes. Lastly, we consider the strengths and weaknesses of mouse models of DS based on the number and nature of the Hsa21 orthologs that are, and are not, trisomic in each, and discuss their validity for use in preclinical evaluations of drug responses.
Language	English
Publishing date	2016-12
Publishing country	United States
Document type	Review ; Journal Article
ZDB-ID	1058547-3
ISSN	1432-1777 ; 0938-8990
ISSN (online)	1432-1777
ISSN	0938-8990
DOI	10.1007/s00335-016-9661-8
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