Effect of cortisol levels on working memory performance in elderly subjects with Alzheimer's disease

Souza-Talarico, Juliana Nery de; Caramelli, Paulo; Nitrini, Ricardo; Chaves, Eliane Corrêa

doi:10.1590/s0004-282x2008000500003

Cited by 15 publications

(11 citation statements)

References 23 publications

(27 reference statements)

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“…There is growing evidence that the effects of physical and psychosocial stressors on the HPA axis may be implicated in the onset and progression of AD [8, 40–42]. For instance, increases in plasma cortisol levels have been reported in patients diagnosed with AD [43–46].…”

Section: Stress and Alzheimer’s Diseasementioning

confidence: 99%

“…Thioflavin S fluorescence stains indicate that relatively smaller sizes of Aβ-plaques were distributed in the cortex (panel A and D), hippocampus (panel B and E), even in the stratum (panel C) [40, 80] after 6 months of isolation stress in the Tg+ mice brain, which were rare in Tg+ mice in age-matched group-housed controls. ELISA analysis indicates Aβ 1–40 and Aβ 1–42 levels in brain tissue were significantly increased in Aβ 1–40 (panel F) and Aβ 1–42 (panel G) in the 6 months isolation-stressed Tg+ mice as compared with group-housed Tg+ mice at the same age [87].…”

Section: Figuresmentioning

confidence: 99%

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Effects of Stress and Stress Hormones on Amyloid-β Protein and Plaque Deposition

Dong

Csernansky

2009

JAD

116

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Growing evidence indicates that physical and psychosocial stressors, in part acting through the hypothalamic-pituitary-adrenal (HPA) axis, may accelerate the process of Alzheimer's disease (AD). In this review, we summarize recent research related to the effects of stress and stress hormones on the various disease process elements associated with AD. Specifically, we focus on the relationships among chronic stressors, HPA axis activity, amyloid-β protein, and amyloid-β plaque deposition in mouse models of AD. The potential mechanisms by which stress and stress-related components, especially corticotrophin-releasing factor and its receptors, influence the pathogenesis of AD are discussed.

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Section: Stress and Alzheimer’s Diseasementioning

confidence: 99%

Section: Figuresmentioning

confidence: 99%

Effects of Stress and Stress Hormones on Amyloid-β Protein and Plaque Deposition

Dong

Csernansky

2009

JAD

116

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“…CRF is also synthesized locally in response to stress in which it stimulates excitatory neurotransmission also via CRFR1, thereby mediating a range of functions necessary for adaptation [8] and relevant to AD, such as cognition, neuroprotection, neuroinflammation, amyloid, and tau processing [9]. Postmortem observation of AD brains has revealed altered CRF and CRFR1 levels in the hypothalamus and other brain areas [9], together with increased circulating levels of glucocorticoids [10].…”

Section: Introductionmentioning

confidence: 99%

Corticotropin-Releasing Factor Receptor 1 Activation During Exposure to Novelty Stress Protects Against Alzheimer's Disease-Like Cognitive Decline in AβPP/PS1 Mice

Scullion

Hewitt

Pardon

2013

JAD

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A lifestyle rich in physical and mental activities protects against Alzheimer's disease (AD) but the underlying mechanisms are unclear. We have proposed that this is mediated by a stress response and have shown that repeated exposure to novelty stress, which induces physical and exploratory activities, delays the progression of AD-like pathology in the TASTPM mouse model. Here, we aimed to establish the role played by corticotrophin-releasing factor receptor 1 (CRFR1), a major component of the stress axis, in TASTPM's behavioral and neuroendocrine responses to novelty and related protective effects. We show that the stress response of TASTPM mice is altered with reduced CRFR1-mediated neuroendocrine and behavioral responses to novelty and a distinct profile of behavioral responses. Repeated novelty-induced CRFR1 activation, however, mediated the improved contextual fear memory and extinction performance of TASTPM mice and increased hippocampal and fronto-cortical levels of synaptophysin, a marker of synaptic density, and fronto-cortical levels of the post-synaptic marker PSD95. The N-methyl-D-aspartate receptor (NMDAR) is the major receptor for synaptic plasticity underlying learning and memory. Although novelty-induced NMDAR activation contributed to enhancement of fear memory and synaptophysin levels, antagonism of CRFR1 and NMDAR prevented the novelty-induced increase in hippocampal synaptophysin levels but reversed the other effects of CRFR1 inactivation, i.e., the enhancement of contextual fear extinction and fronto-cortical synaptophysin and PSD95 levels. These findings suggest a novel mechanism whereby a stimulating environment can delay AD symptoms through CRFR1 activation, facilitating NMDAR-mediated synaptic plasticity and synaptogenesis in a region-dependent manner, either directly, or indirectly, by modulating PSD95.

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“…Alzheimer's disease (AD) is a chronic neurodegenerative disease characterized by cognitive difficulties and memory and executive dysfunction . In neurodegenerative disorders, neuronal systems are progressively affected .…”

Section: Introductionmentioning

confidence: 99%

Evaluation of salivary acetylcholinesterase and pseudocholinesterase in patients with Alzheimer's disease: A case–control study

Ahmadi‐Motamayel

Goodarzi

Tarazi

et al. 2018

Special Care in Dentistry

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Aim:The aim of this study was to evaluate acetylcholinesterase (AChE) and pseudocholinesterase (PChE) in whole saliva in patients with Alzheimer's disease (AD) and in healthy subjects. Saliva has a high potential for keeping track of general health and diseases. AD is a type of dementia with reduction in brain cholinergic markers that causes memory, thinking, and behavior problems. Up to 90% decrease in AChE activity has been observed in AD. Methods and results:Thirty healthy subjects and 30 patients with AD participated in this study. Saliva samples were collected from 8 to 10 AM. AChE and PChE of saliva were assessed by the Ellman method. Statistical comparison was performed using SPSS 16 for t-test. The activity of AChE and PChE significantly increased in the group with AD compared to the healthy subjects. Sex had no effect on the activities of these enzymes. No correlation existed between the duration of illness and enzymatic activity. The enzyme levels reduced with age.Conclusion: AChE and PChE levels were increased in saliva samples of patients with AD. Therefore, saliva has the potential for being used for the purpose of biomarker evaluation to replace cerebrospinal fluid in patients with AD.

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Effect of cortisol levels on working memory performance in elderly subjects with Alzheimer's disease

Cited by 15 publications

References 23 publications

Effects of Stress and Stress Hormones on Amyloid-β Protein and Plaque Deposition

Effects of Stress and Stress Hormones on Amyloid-β Protein and Plaque Deposition

Corticotropin-Releasing Factor Receptor 1 Activation During Exposure to Novelty Stress Protects Against Alzheimer's Disease-Like Cognitive Decline in AβPP/PS1 Mice

Evaluation of salivary acetylcholinesterase and pseudocholinesterase in patients with Alzheimer's disease: A case–control study

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