Repeated novel cage exposure-induced improvement of early Alzheimer's-like cognitive and amyloid changes in TASTPM mice is unrelated to changes in brain endocannabinoids levels

Pardon, Marie‐Christine; Sarmad, Sarir; Rattray, Ivan; Bates, Timothy E.; Scullion, Gillian; Marsden, C.A.; Lowe, James; Kendall, David A.

doi:10.1016/j.neurobiolaging.2007.10.002

Cited by 37 publications

(37 citation statements)

References 55 publications

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“…Also as expected, in view of findings with the hyperactive phenotype, this pattern appears age-related, at least with respect to APP 695 SWE+ PS1 /M146L/ Thy1 mutants, found to be hypoactive at 10 months of age (Pugh et al, 2007) but not at 4 (Pardon et al, 2009). …”

Section: Exploratory Activity In Alzheimer Micesupporting

confidence: 82%

APP transgenic mice for modelling behavioural and psychological symptoms of dementia (BPSD)

Lalonde

Fukuchi

Strazielle

2012

Neuroscience & Biobehavioral Reviews

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The discovery of gene mutations responsible for autosomal dominant Alzheimer's disease has enabled researchers to reproduce in transgenic mice several hallmarks of this disorder, notably Aβ accumulation, though in most cases without neurofibrillary tangles. Mice expressing mutated and wild-type APP as well as C-terminal fragments of APP exhibit variations in exploratory activity reminiscent of behavioral and psychological symptoms of Alzeimer dementia (BPSD). In particular, open-field, spontaneous alternation, and elevated plus-maze tasks as well as aggression are modified in several APP transgenic mice relative to non-transgenic controls. However, depending on the precise murine models, changes in open-field and elevated plus-maze exploration occur in either direction, either increased or decreased relative to controls. It remains to be determined which neurotransmitter changes are responsible for this variability, in particular with respect to GABA, 5HT, and dopamine.

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Section: Exploratory Activity In Alzheimer Micesupporting

confidence: 82%

APP transgenic mice for modelling behavioural and psychological symptoms of dementia (BPSD)

Lalonde

Fukuchi

Strazielle

2012

Neuroscience & Biobehavioral Reviews

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“…This effect could be attributed to the overall adaptive mechanisms that are triggered by mild stress in order to enable the organism to maintain homeostasis [67]. In support of this notion are the findings of several previous studies indicating the beneficial impact of short-term mild stress in various disease states including cancer, immune diseases [68], Alzheimer's disease [69] and in situations that trigger oxidative damage [70]. Nonetheless, the long term detrimental effects of chronic stress should not be underestimated as it has long been considered as a crucial causative factor in the development of a myriad of diseases including those related to lipid and carbohydrate metabolism, with cardiovascular disorders and obesity holding significant portions of the stress-induced morbidity [2], [3], [5], [10].…”

Section: Discussionmentioning

confidence: 77%

Role of PPARα and HNF4α in Stress-Mediated Alterations in Lipid Homeostasis

et al. 2013

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Stress is a risk factor for several cardiovascular pathologies. PPARα holds a fundamental role in control of lipid homeostasis by directly regulating genes involved in fatty acid transport and oxidation. Importantly, PPARα agonists are effective in raising HDL-cholesterol and lowering triglycerides, properties that reduce the risk for cardiovascular diseases. This study investigated the role of stress and adrenergic receptor (AR)-related pathways in PPARα and HNF4α regulation and signaling in mice following repeated restraint stress or treatment with AR-antagonists administered prior to stress to block AR-linked pathways. Repeated restraint stress up-regulated Pparα and its target genes in the liver, including Acox, Acot1, Acot4, Cyp4a10, Cyp4a14 and Lipin2, an effect that was highly correlated with Hnf4α. In vitro studies using primary hepatocyte cultures treated with epinephrine or AR-agonists confirmed that hepatic AR/cAMP/PKA/CREB- and JNK-linked pathways are involved in PPARα and HNF4α regulation. Notably, restraint stress, independent of PPARα, suppressed plasma triglyceride levels. This stress-induced effect could be attributed in part to hormone sensitive lipase activation in the white adipose tissue, which was not prevented by the increased levels of perilipin. Overall, this study identifies a mechanistic basis for the modification of lipid homeostasis following stress and potentially indicates novel roles for PPARα and HNF4α in stress-induced lipid metabolism.

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“…The environmental enrichment procedures provide social interactions, cognitive stimulation, exposure to novelty, and increased motor activity. Previous research indicates a major role for cognitive stimulation (Cracchiolo, et al, 2007; Harburger, et al, 2007; Marques, et al, 2009; Pietropaolo, et al, 2006) and novelty (Pardon, et al, 2009; Veyrac, et al, 2009) in improving spatial learning and memory, with a relatively minor influence of social interactions (Diniz, et al, 2010; Schrijver, et al, 2002; Schrijver, et al, 2004; Winocur, 1998). Motor activity interacts with the other variable such that improved memory is observed when motor activity occurs in an environment that is separate from the home cage or requires extensive handling (Harburger, et al, 2007; Lambert, et al, 2005; O'Callaghan, et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

Influence of late-life exposure to environmental enrichment or exercise on hippocampal function and CA1 senescent physiology

Kumar

Rani

Tchigranova

et al. 2012

Neurobiology of Aging

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Aged (20–22 months) male Fischer 344 rats were randomly assigned to sedentary (A-SED), environmentally enriched (A-ENR) or exercise (A-EX) conditions. After 10–12 weeks of differential experience, the three groups of aged rats and young sedentary controls were tested for physical and cognitive function. Spatial discrimination learning and memory consolidation, tested on the water maze, were enhanced in A-ENR compared to A-SED. A-EX exhibited improved and impaired performance on the cue and spatial task, respectively. Impaired spatial learning in A-EX was likely due to a bias in response selection associated with exercise training, as object recognition memory improved for A-EX rats. An examination of senescent hippocampal physiology revealed that enrichment and exercise reversed age-related changes in long-term depression (LTD) and long-term potentiation (LTP). Rats in the enrichment group exhibited an increase in cell excitability compared to the other two groups of aged animals. The results indicate that differential experience biased the selection of a spatial or a response strategy and factors common across the two conditions, such as increased hippocampal activity associated with locomotion, contribute to reversal of senescent synaptic plasticity.

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Repeated novel cage exposure-induced improvement of early Alzheimer's-like cognitive and amyloid changes in TASTPM mice is unrelated to changes in brain endocannabinoids levels

Cited by 37 publications

References 55 publications

APP transgenic mice for modelling behavioural and psychological symptoms of dementia (BPSD)

APP transgenic mice for modelling behavioural and psychological symptoms of dementia (BPSD)

Role of PPARα and HNF4α in Stress-Mediated Alterations in Lipid Homeostasis

Influence of late-life exposure to environmental enrichment or exercise on hippocampal function and CA1 senescent physiology

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