An Integrated Review of Psychological Stress in Parkinson’s Disease: Biological Mechanisms and Symptom and Health Outcomes

Austin, Kim Wieczorek; Ameringer, Suzanne; Cloud, Leslie J.

doi:10.1155/2016/9869712

Cited by 23 publications

(26 citation statements)

References 75 publications

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“…In our conceptual framework, a stressor is considered as any perceived or actual threat to an individual that has the capacity to disrupt homeostasis and cause stress [59]. Most people experience acute stress in response to a stressful event over the life course; however, chronic stress may be more problematic since it can increase one’s risk for several health problems like heart disease [60], neurologic and psychiatric diseases [61], Parkinson’s disease [62], Alzheimer’s disease [63], multiple sclerosis [64], eating disorders [65], addictions [66], post-traumatic stress disorder (PTSD) [67], and sleeping complications [68].…”

Section: Resiliency-stressor Conceptual Framework Componentsmentioning

confidence: 99%

Hybrid Resiliency-Stressor Conceptual Framework for Informing Decision Support Tools and Addressing Environmental Injustice and Health Inequities

Burwell-Naney

Wilson

Whitlock

et al. 2019

IJERPH

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While structural factors may drive health inequities, certain health-promoting attributes of one’s “place” known as salutogens may further moderate the cumulative impacts of exposures to socio-environmental stressors that behave as pathogens. Understanding the synergistic relationship between socio-environmental stressors and resilience factors is a critical component in reducing health inequities; however, the catalyst for this concept relies on community-engaged research approaches to ultimately strengthen resiliency and promote health. Furthermore, this concept has not been fully integrated into environmental justice and cumulative risk assessment screening tools designed to identify geospatial variability in environmental factors that may be associated with health inequities. As a result, we propose a hybrid resiliency-stressor conceptual framework to inform the development of environmental justice and cumulative risk assessment screening tools that can detect environmental inequities and opportunities for resilience in vulnerable populations. We explore the relationship between actual exposures to socio-environmental stressors, perceptions of stressors, and one’s physiological and psychological stress response to environmental stimuli, which collectively may perpetuate health inequities by increasing allostatic load and initiating disease onset. This comprehensive framework expands the scope of existing screening tools to inform action-based solutions that rely on community-engaged research efforts to increase resiliency and promote positive health outcomes.

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Section: Resiliency-stressor Conceptual Framework Componentsmentioning

confidence: 99%

Hybrid Resiliency-Stressor Conceptual Framework for Informing Decision Support Tools and Addressing Environmental Injustice and Health Inequities

Burwell-Naney

Wilson

Whitlock

et al. 2019

IJERPH

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“…The relationship between psychological stress and onset of neurodegenerative disease is not an unexplored one. For example, links between stress and Parkinson disease (PD) have been proposed ( Djamshidian and Lees, 2014 ; Austin et al, 2016 ), and refuted ( Clark et al, 2013 ). However, a prospective study that examined vagal tone indicated by vagally mediated HRV in relation to risk of PD showed that low vagal tone was associated with higher risk of PD 18 years later ( Alonso et al, 2015 ).…”

Section: Applying the Model: Neurodegenerative Disease And Cancermentioning

confidence: 99%

The Neuro-Immuno-Senescence Integrative Model (NISIM) on the Negative Association Between Parasympathetic Activity and Cellular Senescence

2018

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There is evidence that accumulated senescent cells drive age-related pathologies, but the antecedents to the cellular stressors that induce senescence remain poorly understood. Previous research suggests that there is a relationship between shorter telomere length, an antecedent to cellular senescence, and psychological stress. Existing models do not sufficiently account for the specific pathways from which psychological stress regulation is converted into production of reactive oxygen species. We propose the neuro-immuno-senescence integrative model (NISIM) suggesting how vagally mediated heart rate variability (HRV) might be related to cellular senescence. Prefrontally modulated, and vagally mediated cortical influences on the autonomic nervous system, expressed as HRV, affects the immune system by adrenergic stimulation and cholinergic inhibition of cytokine production in macrophages and neutrophils. Previous findings indicate that low HRV is associated with increased production of the pro-inflammatory cytokines IL-6 and TNF-α. IL-6 and TNF-α can activate the NFκB pathway, increasing production of reactive oxygen species that can cause DNA damage. Vagally mediated HRV has been related to an individual’s ability to regulate stress, and is lower in people with shorter telomeres. Based on these previous findings, the NISIM suggest that the main pathway from psychological stress to individual differences in oxidative telomere damage originates in the neuroanatomical components that modulate HRV, and culminates in the cytokine-induced activation of NFκB. Accumulated senescent cells in the brain is hypothesized to promote age-related neurodegenerative disease, and previous reports suggest an association between low HRV and onset of Alzheimer’s and Parkinson’s disease. Accumulating senescent cells in peripheral tissues secreting senescence-associated secretory phenotype factors can alter tissue structure and function which can induce cancer and promote tumor growth and metastasis in old age, and previous research suggested that ability to regulate psychological stress has a negative association with cancer onset. We therefore conclude that the NISIM can account for a large proportion of the individual differences in the psychological stress-related antecedents to cellular senescence, and suggest that it can be useful in providing a dynamic framework for understanding the pathways by which psychological stress induce pathologies in old age.

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“…Glucocorticoids play an important role in regulating microglial activation and proinflammatory cytokine transcription factor expression and release . Dysregulation of this system has been found to cause neuroinflammation, oxidative stress, and loss of dopamine‐producing neurons within the CNS . Although little is known with respect to the effect of chronic stress on PD‐associated constipation, stress is known to contribute to the onset and/or severity of GI dysfunction in the general population …”

Section: Introductionmentioning

confidence: 99%

Chronic isolation stress is associated with increased colonic and motor symptoms in the A53T mouse model of Parkinson’s disease

Diwakarla

Finkelstein

Constable

et al. 2019

Neurogastroenterology Motil

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Background Chronic stress exacerbates motor deficits and increases dopaminergic cell loss in several rodent models of Parkinson's disease (PD). However, little is known about effects of stress on gastrointestinal (GI) dysfunction, a common non‐motor symptom of PD. We aimed to determine whether chronic stress exacerbates GI dysfunction in the A53T mouse model of PD and whether this relates to changes in α‐synuclein distribution. Methods Chronic isolation stress was induced by single‐housing WT and homozygote A53T mice between 5 and 15 months of age. GI and motor function were compared with mice that had been group‐housed. Key Results Chronic isolation stress increased plasma corticosterone and exacerbated deficits in colonic propulsion and whole‐gut transit in A53T mice and also increased motor deficits. However, our results indicated that the novel environment‐induced defecation response, a common method used to evaluate colorectal function, was not a useful test to measure exacerbation of GI dysfunction, most likely because of the reported reduced level of anxiety in A53T mice. A53T mice had lower corticosterone levels than WT mice under both housing conditions, but single‐housing increased levels for both genotypes. Enteric neuropathy was observed in aging A53T mice and A53T mice had a greater accumulation of alpha‐synuclein (αsyn) in myenteric ganglia under both housing conditions. Conclusions & Inferences Chronic isolation stress exacerbates PD‐associated GI dysfunction, in addition to increasing motor deficits. However, these changes in GI symptoms are not directly related to corticosterone levels, worsened enteric neuropathy, or enteric αsyn accumulation.

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An Integrated Review of Psychological Stress in Parkinson’s Disease: Biological Mechanisms and Symptom and Health Outcomes

Cited by 23 publications

References 75 publications

Hybrid Resiliency-Stressor Conceptual Framework for Informing Decision Support Tools and Addressing Environmental Injustice and Health Inequities

Hybrid Resiliency-Stressor Conceptual Framework for Informing Decision Support Tools and Addressing Environmental Injustice and Health Inequities

The Neuro-Immuno-Senescence Integrative Model (NISIM) on the Negative Association Between Parasympathetic Activity and Cellular Senescence

Chronic isolation stress is associated with increased colonic and motor symptoms in the A53T mouse model of Parkinson’s disease

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