scholarly journals The HSA21 gene EURL/C21ORF91 controls neurogenesis within the cerebral cortex and is implicated in the pathogenesis of Down Syndrome

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Shan Shan Li ◽  
Zhengdong Qu ◽  
Matilda Haas ◽  
Linh Ngo ◽  
You Jeong Heo ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Cerebral Cortex ◽  
Hsa21 Gene

Neuronal Compensation and Plasticity in the Cerebral Cortex of Down Syndrome Associated with Mental Retardation and Dementia

2011 ◽  
Vol 26 (3) ◽  
pp. 347-352
Author(s):  
Miwa TAKASHIMA ◽  
Satoru KAI ◽  
Seiichiro TAKAHASHI ◽  
Takafumi FUJIMOTO ◽  
Masahiro YOKOO ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Cerebral Cortex ◽  
Mental Retardation

Apoptosis is directly related to intracellular amyloid accumulation in a cell line derived from the cerebral cortex of a trisomy 16 mouse, an animal model of Down syndrome

2010 ◽  
Vol 470 (1) ◽  
pp. 81-85 ◽  
Author(s):  
Christian Arriagada ◽  
Miguel Bustamante ◽  
Illani Atwater ◽  
Eduardo Rojas ◽  
Raúl Caviedes ◽  
...  
Keyword(s):  
Animal Model ◽  
Down Syndrome ◽  
Cerebral Cortex ◽  
Cell Line ◽  
Trisomy 16 ◽  
Amyloid Accumulation ◽  
A Cell

Altered Voltage Dependent Calcium Currents in a Neuronal Cell Line Derived From the Cerebral Cortex of a Trisomy 16 Fetal Mouse, an Animal Model of Down Syndrome

2011 ◽  
Vol 22 (1) ◽  
pp. 59-68 ◽  
Author(s):  
Mario A. Acuña ◽  
Ramón Pérez-Nuñez ◽  
Jorge Noriega ◽  
Ana María Cárdenas ◽  
Juan Bacigalupo ◽  
...  
Keyword(s):  
Animal Model ◽  
Down Syndrome ◽  
Cerebral Cortex ◽  
Cell Line ◽  
Neuronal Cell ◽  
Calcium Currents ◽  
Trisomy 16 ◽  
Fetal Mouse ◽  
Neuronal Cell Line ◽  
Voltage Dependent

Knockdown of amyloid precursor protein normalizes cholinergic function in a cell line derived from the cerebral cortex of a trisomy 16 mouse: An animal model of down syndrome

2006 ◽  
Vol 84 (6) ◽  
pp. 1303-1310 ◽  
Author(s):  
Patricia Opazo ◽  
Katherine Saud ◽  
Michelle de Saint Pierre ◽  
Ana María Cárdenas ◽  
David D. Allen ◽  
...  
Keyword(s):  
Animal Model ◽  
Down Syndrome ◽  
Cerebral Cortex ◽  
Amyloid Precursor Protein ◽  
Cell Line ◽  
Precursor Protein ◽  
Trisomy 16 ◽  
Cholinergic Function ◽  
A Cell

The cerebral cortex in Fetal Down Syndrome

2003 ◽  
pp. 159-163 ◽  
Author(s):  
U. Unterberger ◽  
G. Lubec ◽  
M. Dierssen ◽  
G. Stoltenburg-Didinger ◽  
J. C. Farreras ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Cerebral Cortex

Aberrant protein expression in cerebral cortex of fetus with Down syndrome

Neuroscience ◽  
2003 ◽  
Vol 122 (1) ◽  
pp. 145-154 ◽  
Author(s):  
E Engidawork ◽  
T Gulesserian ◽  
M Fountoulakis ◽  
G Lubec
Keyword(s):  
Down Syndrome ◽  
Cerebral Cortex ◽  
Protein Expression ◽  
Aberrant Protein

scholarly journals Coat Color-Facilitated Efficient Generation and Analysis of a Mouse Model of Down Syndrome Triplicated for All Human Chromosome 21 Orthologous Regions

Genes ◽  
2021 ◽  
Vol 12 (8) ◽  
pp. 1215
Author(s):  
Yichen Li ◽  
Zhuo Xing ◽  
Tao Yu ◽  
Annie Pao ◽  
Marcel Daadi ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Human Chromosome ◽  
Coat Color ◽  
Gene Dosage ◽  
Chromosome 21 ◽  
Complete Model ◽  
Hsa21 Gene ◽  
Human Chromosome 21 ◽  
Compound Model ◽  
Gene Orthologs

Down syndrome (DS) is one of the most complex genetic disorders in humans and a leading genetic cause of developmental delays and intellectual disabilities. The mouse remains an essential model organism in DS research because human chromosome 21 (Hsa21) is orthologously conserved with three regions in the mouse genome. Recent studies have revealed complex interactions among different triplicated genomic regions and Hsa21 gene orthologs that underlie major DS phenotypes. Because we do not know conclusively which triplicated genes are indispensable in such interactions for a specific phenotype, it is desirable that all evolutionarily conserved Hsa21 gene orthologs are triplicated in a complete model. For this reason, the Dp(10)1Yey/+;Dp(16)1Yey/+;Dp(17)1Yey/+ mouse is the most complete model of DS to reflect gene dosage effects because it is the only mutant triplicated for all Hsa21 orthologous regions. Recently, several groups have expressed concerns that efforts needed to generate the triple compound model would be so overwhelming that it may be impractical to take advantage of its unique strength. To alleviate these concerns, we developed a strategy to drastically improve the efficiency of generating the triple compound model with the aid of a targeted coat color, and the results confirmed that the mutant mice generated via this approach exhibited cognitive deficits.

scholarly journals Metabolic profiling of neurospheres derived from E15.5 cerebral cortex of Ts1Cje mouse model for Down syndrome

2016 ◽  
Vol 10 ◽  
Author(s):  
Seth Eryse ◽  
Lee Han Chung ◽  
Yusof Hadri ◽  
Ling King Hwa ◽  
Cheah Pike See
Keyword(s):  
Down Syndrome ◽  
Cerebral Cortex ◽  
Mouse Model ◽  
Metabolic Profiling
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