Skip header and navigation

Refine By

2 records – page 1 of 1.

15q11.2 CNV affects cognitive, structural and functional correlates of dyslexia and dyscalculia.

https://arctichealth.org/en/permalink/ahliterature287813
Source
Transl Psychiatry. 2017 Apr 25;7(4):e1109
Publication Type
Article
Date
Apr-25-2017
Author
M O Ulfarsson
G B Walters
O. Gustafsson
S. Steinberg
A. Silva
O M Doyle
M. Brammer
D F Gudbjartsson
S. Arnarsdottir
G A Jonsdottir
R S Gisladottir
G. Bjornsdottir
H. Helgason
L M Ellingsen
J G Halldorsson
E. Saemundsen
B. Stefansdottir
L. Jonsson
V K Eiriksdottir
G R Eiriksdottir
G H Johannesdottir
U. Unnsteinsdottir
B. Jonsdottir
B B Magnusdottir
P. Sulem
U. Thorsteinsdottir
E. Sigurdsson
D. Brandeis
A. Meyer-Lindenberg
H. Stefansson
K. Stefansson
Source
Transl Psychiatry. 2017 Apr 25;7(4):e1109
Date
Apr-25-2017
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Chromosome Aberrations
Chromosome Deletion
Chromosomes, Human, Pair 15 - genetics
Cognition - physiology
DNA Copy Number Variations - genetics
Developmental Disabilities - genetics
Dyscalculia - genetics
Dyslexia - genetics
Female
Functional Neuroimaging - methods - standards
Heterozygote
Humans
Iceland - epidemiology
Intellectual Disability - genetics
Magnetic Resonance Imaging - methods
Male
Middle Aged
Neuropsychological Tests - standards
Phenotype
Temporal Lobe - anatomy & histology - diagnostic imaging
Young Adult
Abstract
Several copy number variants have been associated with neuropsychiatric disorders and these variants have been shown to also influence cognitive abilities in carriers unaffected by psychiatric disorders. Previously, we associated the 15q11.2(BP1-BP2) deletion with specific learning disabilities and a larger corpus callosum. Here we investigate, in a much larger sample, the effect of the 15q11.2(BP1-BP2) deletion on cognitive, structural and functional correlates of dyslexia and dyscalculia. We report that the deletion confers greatest risk of the combined phenotype of dyslexia and dyscalculia. We also show that the deletion associates with a smaller left fusiform gyrus. Moreover, tailored functional magnetic resonance imaging experiments using phonological lexical decision and multiplication verification tasks demonstrate altered activation in the left fusiform and the left angular gyri in carriers. Thus, by using convergent evidence from neuropsychological testing, and structural and functional neuroimaging, we show that the 15q11.2(BP1-BP2) deletion affects cognitive, structural and functional correlates of both dyslexia and dyscalculia.
Notes
Cites: Psychol Bull. 2005 Jul;131(4):592-61716060804
Cites: Neuroimage. 2009 Feb 1;44(3):1103-1219027075
Cites: Trends Neurosci. 2001 Sep;24(9):508-1111506881
Cites: J Learn Disabil. 2013 Nov-Dec;46(6):549-6923572008
Cites: Neuroimage. 2011 Aug 1;57(3):742-920884362
Cites: Cogn Neuropsychol. 2003 May 1;20(3):487-50620957581
Cites: Genet Med. 2013 Jun;15(6):478-8123258348
Cites: Neuroimage. 2009 Oct 1;47(4):1940-919446640
Cites: Brain. 2000 Feb;123 ( Pt 2):291-30710648437
Cites: PLoS One. 2012;7(8):e4312222916214
Cites: Nature. 2015 Apr 9;520(7546):224-925607358
Cites: Proc Biol Sci. 2015 May 7;282(1806):2014313925854887
Cites: Neurology. 2001 Mar 27;56(6):781-311274316
Cites: Mol Psychiatry. 2015 Feb;20(1):140-725421402
Cites: J Neurosci. 2014 Aug 20;34(34):11199-21125143601
Cites: Neuroimage. 1995 Dec;2(4):244-529343609
Cites: Front Hum Neurosci. 2009 Nov 24;3:5120046827
Cites: J Clin Psychiatry. 1998;59 Suppl 20:22-33;quiz 34-579881538
Cites: Science. 2011 May 27;332(6033):1049-5321617068
Cites: Hum Brain Mapp. 2009 Sep;30(9):2936-5219172644
Cites: Nat Genet. 2012 Apr 15;44(5):552-6122504417
Cites: Neuroimage. 2007 Oct 15;38(1):95-11317761438
Cites: Neuroscientist. 2013 Feb;19(1):43-6122547530
Cites: PLoS One. 2012;7(8):e4242222900020
Cites: Genes Brain Behav. 2015 Apr;14(4):369-7625778778
Cites: Nat Neurosci. 2016 Mar;19(3):420-3126854805
Cites: Hum Brain Mapp. 2009 Oct;30(10):3299-30819288465
Cites: Transl Psychiatry. 2014 Mar 25;4:e37424667445
Cites: Stat Methods Med Res. 2003 Oct;12(5):419-4614599004
Cites: J Learn Disabil. 2014 Nov-Dec;47(6):532-4223456983
Cites: Vision Res. 2001;41(10-11):1409-2211322983
Cites: J Neurosci. 1997 Jun 1;17(11):4302-119151747
Cites: Hum Brain Mapp. 2013 Nov;34(11):3055-6522711189
Cites: Neuroimage. 2002 Jan;15(1):273-8911771995
Cites: Brain Res Bull. 2005 Nov 15;67(5):403-1216216687
Cites: Cell Stem Cell. 2014 Jul 3;15(1):79-9124996170
Cites: Neuropsychologia. 2016 Mar;83:48-6226119921
Cites: Ann N Y Acad Sci. 2008 Dec;1145:237-5919076401
Cites: Hum Brain Mapp. 2008 May;29(5):613-2517636558
Cites: Proc Natl Acad Sci U S A. 2010 Apr 27;107(17):7939-4420395549
Cites: Cortex. 2010 Nov-Dec;46(10):1284-9820650450
Cites: J Exp Child Psychol. 2009 Jul;103(3):309-2419398112
Cites: Neuroimage. 2000 Jun;11(6 Pt 1):805-2110860804
Cites: Nature. 2014 Jan 16;505(7483):361-624352232
Cites: Nat Rev Neurosci. 2015 Apr;16(4):234-4425783611
PubMed ID
28440815 View in PubMed
Less detail

Oral administration of transgenic barley expressing a Culicoides allergen induces specific antibody response.

https://arctichealth.org/en/permalink/ahliterature287308
Source
Equine Vet J. 2017 Jul;49(4):512-518
Publication Type
Article
Date
Jul-2017
Author
S. Jonsdottir
V. Svansson
S B Stefansdottir
E. Mäntylä
E. Marti
S. Torsteinsdottir
Source
Equine Vet J. 2017 Jul;49(4):512-518
Date
Jul-2017
Language
English
Publication Type
Article
Keywords
Administration, Oral
Allergens - immunology
Animals
Antibody formation
Ceratopogonidae - immunology
Hordeum - genetics
Horse Diseases - immunology
Horses
Hypersensitivity - veterinary
Iceland
Insect Bites and Stings - immunology - veterinary
Abstract
Insect bite hypersensitivity is an immunoglobulin (Ig)E-mediated dermatitis of horses initiated by bites of midges of the genus Culicoides. Culicoides spp. are not indigenous to Iceland and the prevalence of insect bite hypersensitivity is much higher in horses born in Iceland and exported as compared to Icelandic horses born in a Culicoides rich environment. Immunotherapy is therefore needed.
The aim of the study was to express an allergen from Culicoides in barley grain and investigate whether an immune response could be obtained in healthy Icelandic horses by oral treatment with transgenic barley expressing the allergen.
In vivo experiment.
The allergen was expressed in barley grain with the Orfeus technique. A device was developed to treat horses orally with barley flour. Four Icelandic horses were treated with transgenic barley and 3 with control barley, in total 500 g in 7 feedings. Serum and saliva samples were collected for measuring specific antibodies.
The allergen Cul n 2, a hyaluronidase originating from the salivary gland of Culicoides nubeculosus, was expressed in barley. Horses treated with the transgenic barley mounted a Cul n 2 specific IgG1 and IgG4/7 response in serum and saliva. The serum response was significantly different between the transgenic and control barley treated horses for both subclasses and the saliva response for IgG1. The induced serum antibodies bound to the corresponding allergen from Culicoides obsoletus, rCul o 2 and were able to partially block binding of Cul n 2 as well as Cul o 2 specific IgE from insect bite hypersensitivity affected horses.
Small number of horses.
This study shows that specific antibody response can be induced in horses not exposed to Culicoides, using oral treatment with transgenic barley expressing an allergen. Further studies will determine whether this approach is a useful alternative for prevention and treatment of equine insect bite hypersensitivity.
PubMed ID
27859584 View in PubMed
Less detail