Long-term voluntary running modifies the levels of proteins of the excitatory/inhibitory system and reduces reactive astrogliosis in the brain of Ts65Dn mouse model for Down syndrome

2021 ◽  
pp. 147535
Author(s):  
Elizabeth Kida ◽  
Marius Walus ◽  
Giorgio Albertini ◽  
Adam A. Golabek
Keyword(s):  
Down Syndrome ◽  
Mouse Model ◽  
Ts65dn Mouse ◽  
Inhibitory System ◽  
Reactive Astrogliosis ◽  
Voluntary Running ◽  
The Brain

Short- and long-term effects of neonatal pharmacotherapy with epigallocatechin-3-gallate on hippocampal development in the Ts65Dn mouse model of Down syndrome

Neuroscience ◽  
2016 ◽  
Vol 333 ◽  
pp. 277-301 ◽  
Author(s):  
Fiorenza Stagni ◽  
Andrea Giacomini ◽  
Marco Emili ◽  
Stefania Trazzi ◽  
Sandra Guidi ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Mouse Model ◽  
Long Term Effects ◽  
Ts65dn Mouse ◽  
Short And Long Term ◽  
Hippocampal Development

scholarly journals Long‐term effects of maternal choline supplementation on CA1 pyramidal neuron gene expression in the Ts65Dn mouse model of Down syndrome and Alzheimer's disease

2019 ◽  
Vol 33 (9) ◽  
pp. 9871-9884 ◽  
Author(s):  
Melissa J. Alldred ◽  
Helen M. Chao ◽  
Sang Han Lee ◽  
Judah Beilin ◽  
Brian E. Powers ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Down Syndrome ◽  
Mouse Model ◽  
Pyramidal Neuron ◽  
Long Term Effects ◽  
Ts65dn Mouse ◽  
Ca1 Pyramidal Neuron

scholarly journals Long-term effect of neonatal inhibition of APP gamma-secretase on hippocampal development in the Ts65Dn mouse model of Down syndrome

2017 ◽  
Vol 103 ◽  
pp. 11-23 ◽  
Author(s):  
Fiorenza Stagni ◽  
Alessandra Raspanti ◽  
Andrea Giacomini ◽  
Sandra Guidi ◽  
Marco Emili ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Mouse Model ◽  
Term Effect ◽  
Gamma Secretase ◽  
Ts65dn Mouse ◽  
Long Term Effect ◽  
Hippocampal Development

scholarly journals Behavioral validation of the Ts65Dn mouse model for Down syndrome of a genetic background free of the retinal degeneration mutation Pde6brd1

2010 ◽  
Vol 206 (1) ◽  
pp. 52-62 ◽  
Author(s):  
Alberto C.S. Costa ◽  
Melissa R. Stasko ◽  
Cecilia Schmidt ◽  
Muriel T. Davisson
Keyword(s):  
Down Syndrome ◽  
Mouse Model ◽  
Retinal Degeneration ◽  
Genetic Background ◽  
Ts65dn Mouse ◽  
Behavioral Validation

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

scholarly journals Disrupted interferon-related molecular networks and the over-expressed Ifnar1 in the brain of adult Ts1Cje mouse model of Down syndrome

2016 ◽  
Vol 10 ◽  
Author(s):  
Tan Kai-Leng ◽  
Lee Han-Chung ◽  
Ling King-Hwa ◽  
Scott Hamish. S. ◽  
Lai Mei-I ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Mouse Model ◽  
Molecular Networks ◽  
The Brain

scholarly journals Long-term decreased cannabinoid type-1 receptor activity restores specific neurological phenotypes in the Ts65Dn mouse model of Down syndrome

2021 ◽  
Author(s):  
Anna Vazquez-Oliver ◽  
Silvia Perez-Garcia ◽  
Nieves Pizarro ◽  
Laura Molina-Porcel ◽  
Rafael de la Torre ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Side Effects ◽  
Mouse Model ◽  
Neurological Deficits ◽  
Wild Type ◽  
Male And Female ◽  
Cannabinoid Type 1 Receptor ◽  
Cognitive Improvement

Intellectual disability is the most prevalent and limiting hallmark of Down syndrome (DS), without any pharmacological treatment available. Neurodegeneration and neuroinflammation are relevant neurological features of DS reaching to early development of Alzheimer s disease. Preclinical evidence suggests that the endocannabinoid system, an important neuromodulator on cognition and neuroinflammation, could act as beneficial target in DS. Indeed, cannabinoid type-1 receptor (CB1R) activity was enhanced in the hippocampus of young-adult trisomic Ts65Dn mice, a well-characterized surrogate model of DS. In previous studies, inhibition of CB1R, was able to restore key neurological deficits in this mouse model. To determine the possible clinical relevance of this target, it is mandatory to evaluate the long-term consequences of attenuated CB1R activity and to minimize the possible side-effects associated to this mechanism. We found that CB1R expression was significantly enhanced in the hippocampus brains of aged DS subjects. Similarly, middle-aged trisomic mice showed enhanced CB1R expression. Long-term oral administration of a low dose of the CB1R specific antagonist rimonabant was administered to male and female Ts65Dn trisomic and wild-type mice from the time of weaning to 10 months, an age when signs of neurodegeneration have been described in the model. CB1R inhibition resulted in significant cognitive improvement in novel object-recognition memory in trisomic male and female mice, reaching a similar performance to that of wild-type littermates. Interestingly, this long-term rimonabant treatment modify locomotor activity, anxiety-like behavior, body weight or survival rates. Brain analysis at 10 months of age revealed noradrenergic and cholinergic neurodegeneration signs in trisomic mice that were not modified by the treatment, although the alterations in hippocampal microglia morphology shown by vehicle-treated trisomic mice was normalized in trisomic mice exposed to rimonabant. Altogether, our results demonstrate a sustained pro-cognitive effect of CB1R inhibition at doses that do not produce major side effects that could be associated to an anti-inflammatory action, suggesting a potential interest in this target of to preserve cognitive functionality in DS.

scholarly journals Rapid forgetting of social learning in the Ts65Dn mouse model of Down syndrome: New evidence for hippocampal dysfunction.

2018 ◽  
Vol 132 (1) ◽  
pp. 51-56 ◽  
Author(s):  
Brian E. Powers ◽  
Nicholas A. Santiago ◽  
Barbara J. Strupp
Keyword(s):  
Down Syndrome ◽  
Social Learning ◽  
Mouse Model ◽  
Ts65dn Mouse ◽  
Hippocampal Dysfunction ◽  
New Evidence
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