Poster #S15 A MOUSE MODEL OF 22Q11 DELETION SYNDROME EXHIBITS DEFICITS IN BEHAVIORS RELEVANT TO THE CORE DOMAINS OF SCHIZOPHRENIA

Hughes, Zoe; Graf, Rolf; Hanks, Ashley N.; Lotarski, Susan M.; More, Alexander I.; Rizzo, Stacey Sukoff; Scott, Liam; Stolyar, Polina

doi:10.1016/s0920-9964(14)70294-4

Cited by 1 publication

(2 citation statements)

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“…Earlier studies indicate that 22q11.2DS models with overlapping heterozygote deletions showed impaired ( Stark et al 2008 ; Hughes et al 2014 ) or trends towards impaired ( Sigurdsson et al 2010 ) spatial learning in the T-maze. In agreement with these earlier studies, we saw impaired acquisition learning in this task.…”

Section: Discussionmentioning

confidence: 97%

“…In earlier studies, learning and memory deficits have been reported in 22q11.2DS mouse models. The Df(16)A +/− and Df(16)1+ mutants ( Stark et al 2008 ; Hughes et al 2014 ) had impaired spatial alternation learning in the T-maze although the impairment has not always been replicated ( Sigurdsson et al 2010 ). In the water maze, Df(16)1/+ mice ( Earls et al 2010 ) but not the Df(16)A +/− mutant ( Drew et al 2011 ) showed age-dependent impairments.…”

Section: Introductionmentioning

confidence: 99%

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Assessing the Cognitive Translational Potential of a Mouse Model of the 22q11.2 Microdeletion Syndrome

Nilsson¹,

Fejgin

Gastambide

et al. 2016

Cereb. Cortex

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A chromosomal microdeletion at the 22q11.2 locus is associated with extensive cognitive impairments, schizophrenia and other psychopathology in humans. Previous reports indicate that mouse models of the 22q11.2 microdeletion syndrome (22q11.2DS) may model the genetic basis of cognitive deficits relevant for neuropsychiatric disorders such as schizophrenia. To assess the models usefulness for drug discovery, a novel mouse (Df(h22q11)/+) was assessed in an extensive battery of cognitive assays by partners within the NEWMEDS collaboration (Innovative Medicines Initiative Grant Agreement No. 115008). This battery included classic and touchscreen-based paradigms with recognized sensitivity and multiple attempts at reproducing previously published findings in 22q11.2DS mouse models. This work represents one of the most comprehensive reports of cognitive functioning in a transgenic animal model. In accordance with previous reports, there were non-significant trends or marginal impairment in some tasks. However, the Df(h22q11)/+ mouse did not show comprehensive deficits; no robust impairment was observed following more than 17 experiments and 14 behavioral paradigms. Thus -within the current protocols -the 22q11.2DS mouse model fails to mimic the cognitive alterations observed in human 22q11.2 deletion carriers. We suggest that the 22q11.2DS model may induce liability for cognitive dysfunction with additional "hits" being required for phenotypic expression.

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Section: Discussionmentioning

confidence: 97%