Endogenous Cortisol Exposure and Declarative Verbal Memory

Segerstrom, Suzanne C.; Geiger, Paul J.; Boggero, Ian A.; Schmitt, F.A.; Sephton, Sandra E.

doi:10.1097/psy.0000000000000249

Cited by 18 publications

(21 citation statements)

References 30 publications

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“…8,31 Furthermore, the affective stress of chronic pain may be, as other stressful exposures are, 33,34 implicated in faster cognitive decline via putative cortisol-based pathways. 35,36 If these mechanisms fully explain the accelerated cognitive decline we demonstrate here, resolution of pain would mitigate the detrimental cognitive effects. Classic studies do describe cognitive improvement after initiation of opioid treatment, though these studies were not performed in an elderly population.…”

Section: Discussionmentioning

confidence: 77%

Association Between Persistent Pain and Memory Decline and Dementia in a Longitudinal Cohort of Elders

et al. 2017

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IMPORTANCE Chronic pain is common among the elderly and is associated with cognitive deficits in cross-sectional studies; the population-level association between chronic pain and longitudinal cognition is unknown. OBJECTIVE To determine the population-level association between persistent pain, which may reflect chronic pain, and subsequent cognitive decline. DESIGN, SETTING, AND PARTICIPANTSCohort study with biennial interviews of 10 065 community-dwelling older adults in the nationally representative Health and Retirement Study who were 62 years or older in 2000 and answered pain and cognition questions in both 1998 and 2000. Data analysis was conducted between June 24 and October 31, 2016.EXPOSURES "Persistent pain," defined as a participant reporting that he or she was often troubled with moderate or severe pain in both the 1998 and 2000 interviews. MAIN OUTCOMES AND MEASURESCoprimary outcomes were composite memory score and dementia probability, estimated by combining neuropsychological test results and informant and proxy interviews, which were tracked from 2000 through 2012. Linear mixed-effects models, with random slope and intercept for each participant, were used to estimate the association of persistent pain with slope of the subsequent cognitive trajectory, adjusting for demographic characteristics and comorbidities measures in 2000 and applying sampling weights to represent the 2000 US population. We hypothesized that persistent pain would predict accelerated memory decline and increased probability of dementia. To quantify the impact of persistent pain on functional independence, we combined our primary results with information on the association between memory and ability to manage medications and finances independently. RESULTSOf the 10 065 eligible HRS sample members, 60% were female, and median baseline age was 73 years (interquartile range, 67-78 years). At baseline, persistent pain affected 10.9% of participants and was associated with worse depressive symptoms and more limitations in activities of daily living. After covariate adjustment, persistent pain was associated with 9.2% (95% CI, 2.8%-15.0%) more rapid memory decline compared with those without persistent pain. After 10 years, this accelerated memory decline implied a 15.9% higher relative risk of inability to manage medications and an 11.8% higher relative risk of inability to manage finances independently. Adjusted dementia probability increased 7.7% faster (95% CI, 0.55%-14.2%); after 10 years, this translates to an absolute 2.2% increase in dementia probability for those with persistent pain.CONCLUSIONS AND RELEVANCE Persistent pain was associated with accelerated memory decline and increased probability of dementia.

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Section: Discussionmentioning

confidence: 77%

Association Between Persistent Pain and Memory Decline and Dementia in a Longitudinal Cohort of Elders

et al. 2017

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“…et al, 2008; Ouanes et al, 2017a; Sang et al, 2018). Likewise, most (Beluche et al, 2010; Geerlings et al, 2015; Segerstrom et al, 2016; Ouanes et al, 2017a,b; Echouffo-Tcheugui et al, 2018), even though not all (Lee B.K. et al, 2008) studies exploring the relationship between episodic memory and cortisol levels have found an association between elevated cortisol and poorer episodic memory among older adults without dementia.…”

Section: Glucocorticoid Receptors and Cortisol Effects On Cognitionmentioning

confidence: 99%

High Cortisol and the Risk of Dementia and Alzheimer’s Disease: A Review of the Literature

Ouanes

Popp

2019

Front. Aging Neurosci.

311

212

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Introduction: Cortisol effects on the brain are exerted through two distinct receptors, inducing complex and even opposite effects on the cerebral structures implicated in the various cognitive functions. High cortisol may also have deleterious effects on the brain structures and contribute to neurodegeneration, in particular Alzheimer’s disease (AD), via different mechanisms. Objective: To examine the interrelationships between cortisol, cognitive impairment and AD. Methods: Review of the literature. Results: Clinical studies found that elevated cortisol was associated with poorer overall cognitive functioning, as well as with poorer episodic memory, executive functioning, language, spatial memory, processing speed, and social cognition; while in animals, glucocorticoid administration resulted in cognitive impairment and abnormal behavior. In cognitively healthy subjects, higher cortisol levels have been associated with an increased risk of cognitive decline and AD. Subjects with dementia and Mild Cognitive Impairment (MCI) due to AD have been found to have higher CSF cortisol levels than cognitively healthy controls. Elevated CSF cortisol may also be associated with a more rapid cognitive decline in MCI due to AD. Elevated cortisol levels have been also found in delirium. High cortisol may mediate the impact of stressful life events, high neuroticism, depression, sleep disturbances, as well as cardiovascular risk factors on cognitive performance, neurodegeneration, and cognitive decline. High cortisol may also exert neurotoxic effects on the hippocampus, and promote oxidative stress and amyloid β peptide toxicity. Further possible underlying mechanisms include the interactions of cortisol with inflammatory mediators, neurotransmitters, and growth factors. Conclusion: Elevated cortisol levels may exert detrimental effects on cognition and contribute to AD pathology. Further studies are needed to investigate cortisol-reducing and glucocorticoidreceptor modulating interventions to prevent cognitive decline.

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“…Possibly due to lack of power, the current study may not have observed an effect of cortisol on memory, but future work with larger sample sizes could ascertain whether moderated (age) mediation (HPA-axis functioning) is present. Further, longitudinal evidence indicates that persistent elevated daily cortisol exposure is a better predictor of memory in healthy older adults than single measurements alone (Segerstrom et al, 2016). Antidepressant use in a portion of our sample (n = 22; ~58%) may also contribute to these null results, a notable limitation of the design as it related to the current investigation.…”

Section: Discussionmentioning

confidence: 78%

Examining HPA-axis functioning as a mediator of the relationship between depression and cognition across the adult lifespan

Karstens

Korzun

Avery

et al. 2018

Aging, Neuropsychology, and Cognition

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Altered HPA-axis functioning is a hypothesized mechanism for worsened cognition in depression. The current study examines the indirect effects of depression on processing speed, executive functioning, and memory as a function of the HPA-axis. 38 individuals with a depression diagnosis and 50 healthy controls (HCs) aged 18-86 underwent neuropsychological testing and at-home diurnal salivary cortisol collection. Depression was assessed via structured clinical interviews and rating scales. Cognitive composite scores were derived from factor analysis. Daytime cortisol exposure was estimated using area under the curve (AUC). Depression was associated with higher cortisol levels and slower processing speed . A significant suppression effect of AUC was present on the relationship between depression and processing speed. Limitations include the cross-sectional design and limited sample heterogeneity. Though poorly modulated HPA-axis is one proposed mechanism of cognitive alterations in depression, our results did not support this conclusion for processing speed. Alternative mechanisms should be considered to inform interventions to target cognitive alterations in depression.

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Endogenous Cortisol Exposure and Declarative Verbal Memory

Cited by 18 publications

References 30 publications

Association Between Persistent Pain and Memory Decline and Dementia in a Longitudinal Cohort of Elders

Association Between Persistent Pain and Memory Decline and Dementia in a Longitudinal Cohort of Elders

High Cortisol and the Risk of Dementia and Alzheimer’s Disease: A Review of the Literature

Examining HPA-axis functioning as a mediator of the relationship between depression and cognition across the adult lifespan

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