Detecting spatial memory deficits beyond blindness in tg2576 Alzheimer mice

Yassine, Nour; Lazaris, Anelise; Dorner-Ciossek, Cornelia; Després, Olivier; Meyer, Laurence; Maître, Michel; Mensah‐Nyagan, Ayikoe Guy; Cassel, Jean‐Christophe; Mathis, Chantal

doi:10.1016/j.neurobiolaging.2012.06.016

Cited by 51 publications

(55 citation statements)

References 49 publications

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“…Because most of the behavioral tests require several senses and motor capacities, the physical/motor capacities of mice must be carefully determined. For instance, the olfactory integrity of mice is crucial in social tests [30] and tests requiring odor recognition; the visual capacities are also crucial for tests such as observational fear learning or some spatial memory tests [52,90]. Since some FTD mice also develop motor defects, the involvement of motor function in tests has to be considered.…”

Section: Resultsmentioning

confidence: 99%

Evaluating Behavior in Mouse Models of the Behavioral Variant of Frontotemporal Dementia: Which Test for Which Symptom?

Vernay

Sellal²,

Frydman³

2015

Neurodegener Dis

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The behavioral variant of frontotemporal dementia (bvFTD) is a neurodegenerative disease affecting people in their early sixties, characterized by dramatic changes in individual and social behavior. Despite the heterogeneity in the presentation of the clinical symptoms of bvFTD, some characteristic changes can be highlighted. Social disinhibition, changes in food preferences as well as loss of empathy and apathy are commonly described. This is accompanied by a characteristic and dramatic atrophy of the prefrontal cortex with the accumulation of protein aggregates in the neurons in this area. Several causative mutations in different genes have been discovered, allowing the development of transgenic animal models, especially mouse models. In mice, attention has been focused on the histopathological aspects of the pathology, but now studies are taking interest in assessing the behavioral phenotype of FTD models. Finding the right test corresponding to human symptoms is quite challenging, especially since the frontal cortex is much less developed in mice than in humans. Although challenging, the ability to detect relevant prefrontal cortex impairments in mice is crucial for therapeutic approaches. In this review, we aim to present the approaches that have been used to model the behavioral symptoms of FTD and to explore other relevant approaches to assess behavior involving the prefrontal cortex, as well as the deficits associated with FTD.

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Section: Resultsmentioning

confidence: 99%

Evaluating Behavior in Mouse Models of the Behavioral Variant of Frontotemporal Dementia: Which Test for Which Symptom?

Vernay

Sellal²,

Frydman³

2015

Neurodegener Dis

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show abstract

“…This is exemplified with deficits in NOR [32,[51][52][53][54][55], T-maze [50,[56][57][58][59][60] and Barnes maze [53,[61][62][63] in transgenic AD mice, which express mutant forms of amyloid precursor protein, presenilin and/or mapt (tau) genes [64,65]. It should be noticed, however, that the time course of cognitive decline is specific for each model [66].…”

Section: Discussionmentioning

confidence: 99%

Memory formation and retention are affected in adult miR-132/212 knockout mice

Hernandez-Rapp

Smith

Filali³

et al. 2015

Behavioural Brain Research

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“…novel object location test, place recognition test, or spatial novelty test) (Ennaceur and Meliani, 1992;Yassine et al, 2013). Briefly, mice were first allowed to explore in an open field containing two identical objects (with high contrast intra-arena visual cues) for 3 min (Trial 1 -training trial).…”

Section: Novel Object Placement (Op)mentioning

confidence: 99%

Reversal of age-associated cognitive deficits is accompanied by increased plasticity-related gene expression after chronic antidepressant administration in middle-aged mice

Abdourahman

Tamm

et al. 2015

Pharmacology Biochemistry and Behavior

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Cognitive decline occurs during healthy aging, even in middle-aged subjects, via mechanisms that could include reduced stem cell proliferation, changed growth factor expression and/or reduced expression of synaptic plasticity genes. Although antidepressants alter these mechanisms in young rodents, their effects in older animals are unclear. In middle-aged mice, we examined the effects of a selective serotonin reuptake inhibitor (fluoxetine) and a multimodal antidepressant (vortioxetine) on cognitive and affective behaviors, brain stem cell proliferation, growth factor and gene expression. Twelve-month-old female C57BL/6 mice exhibited impaired visuospatial memory in the novel object placement (location) task associated with reduced expression of several plasticity-related genes. Chronic treatment with vortioxetine, but not fluoxetine, improved visuospatial memory and reduced depression-like behavior in the forced swim test in middle-aged mice. Vortioxetine, but not fluoxetine, increased hippocampal expression of several neuroplasticity-related genes in middle-aged mice (e.g., Nfkb1, Fos, Fmr1, Camk2a, Arc, Shank1, Nlgn2, and Rab3a). Neither drug reversed the age-associated decrease in stem cell proliferation. Hippocampal growth factor levels were not consistent with behavioral outcomes. Thus, a change in the expression of multiple genes involved in neuronal plasticity by antidepressant treatment was associated with improved cognitive function and a reduction in depression-like behavior in middle-aged mice.

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Detecting spatial memory deficits beyond blindness in tg2576 Alzheimer mice

Cited by 51 publications

References 49 publications

Evaluating Behavior in Mouse Models of the Behavioral Variant of Frontotemporal Dementia: Which Test for Which Symptom?

Evaluating Behavior in Mouse Models of the Behavioral Variant of Frontotemporal Dementia: Which Test for Which Symptom?

Memory formation and retention are affected in adult miR-132/212 knockout mice

Reversal of age-associated cognitive deficits is accompanied by increased plasticity-related gene expression after chronic antidepressant administration in middle-aged mice

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