Chronic Psychosocial Stress Exacerbates Impairment of Cognition and Long-Term Potentiation in β-Amyloid Rat Model of Alzheimer's Disease

Srivareerat, Marisa; Tran, Trinh T.; Alzoubi, Karem H.; Alkadhi, Karim A.

doi:10.1016/j.biopsych.2008.08.021

Cited by 114 publications

(155 citation statements)

References 69 publications

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“…It is likely that social isolation led to oxidative stress (Schiavone et al, 2009), which in turn stimulated b-and g-secretase activity (Chan et al, 2009) resulting in increased Ab, which then triggered onset of cognition decline in the APP/PS1 mice. These results are consistent with previous reports showing that stress and glucocorticoids similarly promote APP processing along the amyloidogenic pathway (Catania et al, 2009) resulting in the exacerbation of AD-like neuropathology (Billings et al, 2005;Green et al, 2006;Jeong et al, 2006;Srivareerat et al, 2009).…”

Section: Acceleration Of Memory Impairment By Social Isolationsupporting

confidence: 93%

“…Decrease in membraneassociated p35 reduces a-CaMKII synaptic distribution resulting in the synaptic removal of AMPARs. This hypothesis receives support from recent observations that Ab-induced synaptic expression of AMPARs by reducing a-CaMKII synaptic distribution (Gu et al, 2009) and Ab infusion in combination with intruder psychological stress impaired spatial memory by reducing phosphorylated level of a-CaMKII (Srivareerat et al, 2009).…”

Section: Linking Ab To P35 and Memory Impairmentmentioning

confidence: 52%

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The Involvement of Cdk5 Activator p35 in Social Isolation-Triggered Onset of Early Alzheimer’s Disease-Related Cognitive Deficit in the Transgenic Mice

Hsiao

Chen

et al. 2011

Neuropsychopharmacol

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Epidemiological studies indicate that isolated persons have increased risk of developing Alzheimer's disease (AD). This study investigated the cellular mechanisms of how social isolation influenced amyloid b peptide (Ab) accumulation and affected the severity of AD-associated cognitive decline in a mouse model of AD. Amyloid precursor protein (APP) and presenilin 1 (PS1) double-transgenic (APP/PS1) mice were placed either in isolation or in group from postnatal day 28 and tested for cognitive performance at the age of 3 months with fear-conditioning paradigms. We found that social isolation accelerated impairment of contextual fear memory in the APP/PS1 mice. The magnitude of long-term potentiation in the hippocampal CA1 neurons was significantly lower in the isolated APP/PS1 mice compared with group APP/PS1 and wild-type mice. Hippocampal level of Ab was significantly elevated in the isolated APP/PS1 mice, which was accompanied by an increased calpain activity and p25/p35 ratio. In addition, surface expression of GluR1 subunit of AMPA receptor was decreased by social isolation. The association of p35, and a-CaMKII was significantly less in the isolated APP/PS1 mice indicating that their interaction was impaired. These results suggest that social isolation exacerbates memory deficit by increasing Ab level, leading to the increased calpain activity, conversion of p35 to p25 and decrease in association of p35, a-CaMKII, and GluR1, resulting in the endocytosis of AMPA receptors.

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Section: Acceleration Of Memory Impairment By Social Isolationsupporting

confidence: 93%

Section: Linking Ab To P35 and Memory Impairmentmentioning

confidence: 52%

The Involvement of Cdk5 Activator p35 in Social Isolation-Triggered Onset of Early Alzheimer’s Disease-Related Cognitive Deficit in the Transgenic Mice

Hsiao

Chen

et al. 2011

Neuropsychopharmacol

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“…This is in line with the observations that major stressful events lower the age of onset of familial AD (Mejia et al, 2003). In various preclinical AD models, stress worsens deficits in hippocampus-dependent spatial learning (Catania et al, 2009;Cuadrado-Tejedor et al, 2012;Dong et al, 2004;Jeong et al, 2006;Srivareerat et al, 2009;Tran et al, 2010). These deleterious effects are in part caused by an accelerated accumulation of Ab under stressing conditions (Catania et al, 2009;Cuadrado-Tejedor et al, 2012;Dong et al, 2004;Green et al, 2006;Jeong et al, 2006;Srivareerat et al, 2009).…”

Section: Introductionsupporting

confidence: 87%

“…In various preclinical AD models, stress worsens deficits in hippocampus-dependent spatial learning (Catania et al, 2009;Cuadrado-Tejedor et al, 2012;Dong et al, 2004;Jeong et al, 2006;Srivareerat et al, 2009;Tran et al, 2010). These deleterious effects are in part caused by an accelerated accumulation of Ab under stressing conditions (Catania et al, 2009;Cuadrado-Tejedor et al, 2012;Dong et al, 2004;Green et al, 2006;Jeong et al, 2006;Srivareerat et al, 2009). Stress triggers the release of glucocorticoid hormones (CORT), the major output of the hypothalamopituitary-adrenal axis (HPA).…”

Section: Introductionmentioning

confidence: 99%

Subchronic Glucocorticoid Receptor Inhibition Rescues Early Episodic Memory and Synaptic Plasticity Deficits in a Mouse Model of Alzheimer’s Disease

Lanté

Chafaï

Raymond

et al. 2015

Neuropsychopharmacol

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The early phase of Alzheimer's disease (AD) is characterized by hippocampus-dependent memory deficits and impaired synaptic plasticity. Increasing evidence suggests that stress and dysregulation of the hypothalamo-pituitary-adrenal (HPA) axis, marked by the elevated circulating glucocorticoids, are risk factors for AD onset. How these changes contribute to early hippocampal dysfunction remains unclear. Using an elaborated version of the object recognition task, we carefully monitored alterations in key components of episodic memory, the first type of memory altered in AD patients, in early symptomatic Tg2576 AD mice. We also combined biochemical and ex vivo electrophysiological analyses to reveal novel cellular and molecular dysregulations underpinning the onset of the pathology. We show that HPA axis, circadian rhythm, and feedback mechanisms, as well as episodic memory, are compromised in this early symptomatic phase, reminiscent of human AD pathology. The cognitive decline could be rescued by subchronic in vivo treatment with RU486, a glucocorticoid receptor antagonist. These observed phenotypes were paralleled by a specific enhancement of N-Methyl-D-aspartic acid receptor (NMDAR)-dependent LTD in CA1 pyramidal neurons, whereas LTP and metabotropic glutamate receptor-dependent LTD remain unchanged. NMDAR transmission was also enhanced. Finally, we show that, as for the behavioral deficit, RU486 treatment rescues this abnormal synaptic phenotype. These preclinical results define glucocorticoid signaling as a contributing factor to both episodic memory loss and early synaptic failure in this AD mouse model, and suggest that glucocorticoid receptor targeting strategies could be beneficial to delay AD onset.

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“…Nevertheless, some studies reported reduced basal or synaptic activity after chronic stress (Hu et al, 2010;Li et al, 2011;Quan et al, 2011a,b;Zhang et al, 2011). Most studies using field potential recordings found no change in basal synaptic responses (Bodnoff et al, 1995;Gerges et al, 2001;Pavlides et al, 2002;Alfarez et al, 2003;Aleisa et al, 2006a,b,c;Kessal et al, 2006;Holderbach et al, 2007;Goldwater et al, 2009;Srivareerat et al, 2009;but Dumas et al, 2010;Tran et al, 2011), possibly because the effects are too subtle to be noticed extracellularly or depend on GABAergic transmission (which is also not well captured with field potential recordings). Overall, nearly all studies demonstrate that several weeks of stress either enhance intrinsic/synaptically evoked cell activity or are ineffective in this respect, regardless of the area under investigation.…”

mentioning

confidence: 99%

Unraveling the Time Domains of Corticosteroid Hormone Influences on Brain Activity: Rapid, Slow, and Chronic Modes

2012

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Chronic Psychosocial Stress Exacerbates Impairment of Cognition and Long-Term Potentiation in β-Amyloid Rat Model of Alzheimer's Disease

Cited by 114 publications

References 69 publications

The Involvement of Cdk5 Activator p35 in Social Isolation-Triggered Onset of Early Alzheimer’s Disease-Related Cognitive Deficit in the Transgenic Mice

The Involvement of Cdk5 Activator p35 in Social Isolation-Triggered Onset of Early Alzheimer’s Disease-Related Cognitive Deficit in the Transgenic Mice

Subchronic Glucocorticoid Receptor Inhibition Rescues Early Episodic Memory and Synaptic Plasticity Deficits in a Mouse Model of Alzheimer’s Disease

Unraveling the Time Domains of Corticosteroid Hormone Influences on Brain Activity: Rapid, Slow, and Chronic Modes

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