Fluoxetine rescues deficient neurogenesis in hippocampus of the Ts65Dn mouse model for Down syndrome

Clark, Sarah M.; Schwalbe, Jennifer; Stasko, Melissa R.; Yarowsky, Paul; Costa, Alberto C. S.

doi:10.1016/j.expneurol.2006.02.005

Cited by 136 publications

(132 citation statements)

References 26 publications

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“…At postnatal day 2 cell proliferation in Ts65Dn mice, assessed 2 hours after single injection of bromodeoxyuridine (BrdU) was significantly reduced (Contestabile et al, 2007); similar results were revealed at postnatal day 15 (Bianchi et al, 2010). However in young adult Ts65Dn mice the results are conflicting (Clark et al, 2006;Rueda et al, 2005). Similar procedures in young (3-5 months) Ts65Dn mice shows no difference in hippocampal cell proliferation and survival (Rueda et al, 2005).…”

Section: Neurogenesis In Mouse Models Of Dssupporting

confidence: 61%

“…However, in aged (13-15 months) Ts65Dn mice, cell proliferation in the hippocampus (Rueda et al, 2005) and in the subventricular zone (Bianchi et al, 2010) were significantly reduced. Finally, Clark et al (2006) found a difference in DG neurogenesis in young (2-5 months) Ts65Dn mice. It seems that genetic dissections of mouse partial trisomy 16 (Ts65Dn model) did not restore reduced neurogenesis.…”

Section: Neurogenesis In Mouse Models Of Dsmentioning

confidence: 99%

“…Taking to account that this subject is very important for the neurobiology of DS, only a few papers addressed neurogenesis in mouse models of DS (Bianchi et al, 2010;Chakrabarti et al, 2007;Clark et al, 2006;Contestabile et al, 2007;Lorenzi & Reeves, 2006;Rueda et al, 2005). It was noted that in prenatal and newborn Ts65Dn mice neurogenesis was significantly reduced (Chakrabarti et al, 2007;Contestabile et al, 2007;Lorenzi & Reeves, 2006).…”

Section: Neurogenesis In Mouse Models Of Dsmentioning

confidence: 99%

See 2 more Smart Citations

Deficiency of Adult Neurogenesis in the Ts65Dn Mouse Model of Down Syndrome

Belichenko¹,

Kleschevnikov²

2011

Genetics and Etiology of Down Syndrome

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Section: Neurogenesis In Mouse Models Of Dssupporting

confidence: 61%

Section: Neurogenesis In Mouse Models Of Dsmentioning

confidence: 99%

Section: Neurogenesis In Mouse Models Of Dsmentioning

confidence: 99%

See 1 more Smart Citation

Deficiency of Adult Neurogenesis in the Ts65Dn Mouse Model of Down Syndrome

Belichenko¹,

Kleschevnikov²

2011

Genetics and Etiology of Down Syndrome

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“…146,147 The most intensively studied mouse model of DS is the Ts65Dn line, 148 which summarizes the main hallmarks of the DS phenotype, including characteristic craniofacial abnormalities, impaired spatial and non-spatial learning abilities and attention deficits. [149][150][151][152][153][154] At the cellular level, Ts65Dn mice have a reduced number of hippocampal and cerebellar neurons, 155,156 impaired neurogenesis in the dentate gyrus of the hippocampus in both young and aged adults 157,158 and a prominent reduction in dendritic branching in several brain regions, accompanied by alterations in spine size and shape. 159 It is noteworthy that DS is also associated with reduced hippocampal neurogenesis 160 and volume 161 in humans.…”

Section: Impact Of Ee On the Brain L Baroncelli Et Almentioning

confidence: 99%

Nurturing brain plasticity: impact of environmental enrichment

et al. 2009

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Environmental enrichment (EE) is known to profoundly affect the central nervous system (CNS) at the functional, anatomical and molecular level, both during the critical period and during adulthood. Recent studies focusing on the visual system have shown that these effects are associated with the recruitment of previously unsuspected neural plasticity processes. At early stages of brain development, EE triggers a marked acceleration in the maturation of the visual system, with maternal behaviour acting as a fundamental mediator of the enriched experience in both the foetus and the newborn. In adult brain, EE enhances plasticity in the cerebral cortex, allowing the recovery of visual functions in amblyopic animals. The molecular substrate of the effects of EE on brain plasticity is multi-factorial, with reduced intracerebral inhibition, enhanced neurotrophin expression and epigenetic changes at the level of chromatin structure. These findings shed new light on the potential of EE as a non-invasive strategy to ameliorate deficits in the development of the CNS and to treat neurological disorders.

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“…Integration of knowledge about protein interactions and the hypotheses produced by computational modeling regarding pathway perturbation can be tested in mouse models. These mouse models can be further manipulated by genetic and pharmacological means to verify candidate [31][32][33][34] Treatment with fluoxetine, NGF, an agonist of sonic hedgehog, and estrogen, respectively, were shown to provide improvements. A systematic biological approach will define pathway perturbations and identify new, more effective targets for development of therapeutics.…”

Section: Introductionmentioning

confidence: 99%

The cognitive phenotype of Down syndrome: Insights from intracellular network analysis

2006

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Summary: Down syndrome (DS) is caused by trisomy of chromosome 21. All individuals with DS exhibit some level of cognitive dysfunction. It is generally accepted that these abnormalities are a result of the upregulation of genes encoded by chromosome 21. Many chromosome 21 proteins are known or predicted to function in critical neurological processes, but typically they function as modulators of these processes, not as key regulators. Thus, upregulation in DS is expected to cause only modest perturbations of normal processes. Systematic approaches such as intracellular network construction and analysis have not been generally applied in DS research. Networks can be assembled from highthroughput experiments or by text-mining of experimental literature. We survey some new developments in constructing such networks, focusing on newly developed network analysis methodologies. We propose how these methods could be integrated with creation and manipulation of mouse models of DS to advance our understanding of the perturbed cell signaling pathways in DS. This understanding could lead to potential therapeutics.

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Fluoxetine rescues deficient neurogenesis in hippocampus of the Ts65Dn mouse model for Down syndrome

Cited by 136 publications

References 26 publications

Deficiency of Adult Neurogenesis in the Ts65Dn Mouse Model of Down Syndrome

Deficiency of Adult Neurogenesis in the Ts65Dn Mouse Model of Down Syndrome

Nurturing brain plasticity: impact of environmental enrichment

The cognitive phenotype of Down syndrome: Insights from intracellular network analysis

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