scholarly journals Early neurotrophic pharmacotherapy rescues developmental delay and Alzheimer’s-like memory deficits in the Ts65Dn mouse model of Down syndrome

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Syed Faraz Kazim ◽  
Julie Blanchard ◽  
Riccardo Bianchi ◽  
Khalid Iqbal
Keyword(s):  
Down Syndrome ◽  
Mouse Model ◽  
Developmental Delay ◽  
Memory Deficits ◽  
Ts65dn Mouse

scholarly journals Signalling pathways contributing to learning and memory deficits in the Ts65Dn mouse model of Down Syndrome

2021 ◽  
Author(s):  
Aimée Freeburn ◽  
Robert Gordon Keith Munn
Keyword(s):  
Down Syndrome ◽  
Mouse Model ◽  
Learning And Memory ◽  
Memory Deficits ◽  
Signalling Pathways ◽  
Chromosome 16 ◽  
Ts65dn Mouse ◽  
Electrophysiological Studies

Down syndrome is a genetic trisomic disorder that produces life-long changes in physiology and cognition. Many of the changes in learning and memory seen in Down Syndrome (DS) are reminiscent of disorders involving the hippocampal/entorhinal circuit. Mouse models of DS typically involve trisomy of murine chromosome 16 is homologous for many of the genes triplicated in human trisomy 21, and provide us with good models of changes in, and potential pharmacotherapy for, human DS. Recent careful dissection of the Ts65Dn mouse model of DS has revealed differences in key signalling pathways from the basal forebrain to the hippocampus and associated rhinal cortices, as well as changes in the microstructure of the hippocampus itself. In vivo behavioural and electrophysiological studies have shown that  Ts65Dn animals have difficulties in spatial memory that mirror hippocampal deficits, and have changes in hippocampal electrophysiological phenomenology that may explain these differences, and align with expectations generated from in vitro exploration of this model. Finally, given the existing data, we will examine the possibility for pharmacotherapy for DS, and outline the work that remains to be done to fully understand this system.

Memantine Normalizes Several Phenotypic Features in the Ts65Dn Mouse Model of Down Syndrome

2010 ◽  
Vol 21 (1) ◽  
pp. 277-290 ◽  
Author(s):  
Noemí Rueda ◽  
María Llorens-Martín ◽  
Jesús Flórez ◽  
Elsa Valdizán ◽  
Pradeep Banerjee ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Mouse Model ◽  
Ts65dn Mouse ◽  
Phenotypic Features

Hypothermic responses to 8-OH-DPAT in the Ts65Dn mouse model of Down syndrome

Neuroreport ◽  
2006 ◽  
Vol 17 (8) ◽  
pp. 837-841 ◽  
Author(s):  
Melissa R. Stasko ◽  
Jonah J. Scott-McKean ◽  
Alberto C.S. Costa
Keyword(s):  
Down Syndrome ◽  
Mouse Model ◽  
Ts65dn Mouse

P1-049: Chronic Memantine administration reduces APP expression, normalizes glutamatergic synapse density, and improves spatial learning in the Ts65Dn mouse model for down syndrome

2008 ◽  
Vol 4 ◽  
pp. T220-T220
Author(s):  
Carmen Martı́nez-Cué ◽  
Noemı́ Rueda ◽  
Marı́a Llorens-Martı́n ◽  
Jesús Flórez ◽  
Elsa Valdizán ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Mouse Model ◽  
Spatial Learning ◽  
Glutamatergic Synapse ◽  
Ts65dn Mouse ◽  
Synapse Density

scholarly journals P4-032: GM-CSF REVERSES MEMORY DEFICITS IN NORMAL AGED MICE AND IN THE DP(16)1YEY MOUSE MODEL OF DOWN SYNDROME

2019 ◽  
Vol 15 ◽  
pp. P1286-P1287
Author(s):  
Md. Mahiuddin Ahmed ◽  
Athena Ching Jung Wang ◽  
Timothy Boyd ◽  
Mihret Elos ◽  
Heidi J. Chial ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Mouse Model ◽  
Memory Deficits ◽  
Aged Mice ◽  
Gm Csf
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