Prospects for Improving Brain Function in Individuals with Down Syndrome

@article{Costa2013ProspectsFI,
  title={Prospects for Improving Brain Function in Individuals with Down Syndrome},
  author={Alberto C.S. Costa and Jonah J. Scott-McKean},
  journal={CNS Drugs},
  year={2013},
  volume={27},
  pages={679-702}
}
Down syndrome (DS), which results from an extra copy of chromosome 21 (trisomy 21), is the most common genetically defined cause of intellectual disability. Although no pharmacotherapy aimed at counteracting the cognitive and adaptive deficits associated with this genetic disorder has been approved at present, there have been several new promising studies on pharmacological agents capable of rescuing learning/memory deficits seen in mouse models of DS. Here, we will review the available mouse… 
Timing of therapies for Down syndrome: the sooner, the better
TLDR
This review summarizes what the authors know about the effects of pharmacotherapies during different life stages in mouse models of Down syndrome and gives reason to believe that treatments during pregnancy may rescue brain development in fetuses with DS.
Cognitive Impairment, Neuroimaging, and Alzheimer Neuropathology in Mouse Models of Down Syndrome.
TLDR
The validation of appropriate DS mouse models that mimic neurodegeneration and memory loss in humans with DS can be valuable in the study of novel preventative and treatment interventions, and may be helpful in pinpointing gene-gene interactions as well as specific gene segments involved in neurodegenersation.
PERSPECTIVES ON THE USE OF MOUSE MODELS OF DOWN SYNDROME IN TRANSLATIONAL RESEARCH INVOLVING VISUAL AND MOTOR FUNCTIONS
Down syndrome (DS) is a genetic disorder that results from the presence of one extra chromosome 21 in the cell nucleus (trissomy 21), and is the most frequent cause of intellectual disability of
Long-term effects of neonatal treatment with fluoxetine on cognitive performance in Ts65Dn mice
TLDR
Findings suggest that the enduring outcome of neonatal treatment with fluoxetine may be due to MeCP2-dependent restoration of the 5-HT1A-R, and provide new hope for the therapy of DS.
Short- and long-term effects of neonatal pharmacotherapy with epigallocatechin-3-gallate on hippocampal development in the Ts65Dn mouse model of Down syndrome
TLDR
Findings show that treatment with EGCG carried out in the neonatal period rescues numerous trisomy-linked brain alterations, however, even during this, the most critical time window for hippocampal development, E GCG does not elicit enduring effects on the hippocampal physiology.
Epigallocatechin gallate: A useful therapy for cognitive disability in Down syndrome?
TLDR
Evidence in the Ts65Dn mouse model of DS shows that EGCG restores hippocampal development, although this effect is ephemeral, and protocols of periodic E GCG administration to individuals with DS (alone or in conjunction with other treatments) may prevent the disappearance of its effects.
Pharmacological Rescue of Dendritic Pathology in the Ts65Dn Mouse Model of Down Syndrome
Down syndrome (DS) is a genetic pathology characterized by brain hypotrophy and severe cognitive disability. Although defective neurogenesis is an important determinant of cognitive impairment, a
Treatment with corn oil improves neurogenesis and cognitive performance in the Ts65Dn mouse model of Down syndrome
TLDR
It is shown for the first time that fatty acids have a positive impact on the brain of the Ts65Dn mouse model of DS, suggesting that a diet that is rich in fatty acids may exert beneficial effects on cognitive performance in individuals with DS without causing adverse effects.
Mitochondrial Abnormalities in Down Syndrome: Pathogenesis, Effects and Therapeutic Approaches
TLDR
The working hypothesis is that correcting the mitochondrial defect might improve the neurological phenotype and prevent DS-associated pathologies, thus providing a better quality of life for DS individuals and their families.
Glucagon-Like Peptide-1 Cleavage Product Improves Cognitive Function in a Mouse Model of Down Syndrome
TLDR
It is reported that systemic administration of GLP-1 (9-36) in Ts65Dn DS model mice of either sex resulted in decreased mitochondrial oxidative stress in hippocampus and improved dendritic spine morphology, increase of mature spines and reduction of immature spines.
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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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