Diurnal salivary cortisol concentrations in Parkinson&amp;rsquo;s disease: increased total secretion and morning cortisol concentrations

Skogar, Örjan; Fall, Per-Arne; Hallgren, G; Lökk, Johan; Bringer, B; Carlsson, Magnus; Lennartsson, U; Sandbjörk, Håkan; Cj, Törnhage

doi:10.2147/ijgm.s20875

Cited by 18 publications

(20 citation statements)

References 37 publications

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“…Similarly, elevated serum cortisol levels were reported in a larger collective study of idiopathic and non-idiopathic PD patients compared to controls ( 281 ). It is important to note that cortisol concentrations measured from saliva samples do not reflect any signs of pathology ( 282 ) and this should be a key consideration in the design of future clinical studies. While the inconsistencies between previous plasma profiling studies could be attributed to age, progression of disease or drug treatment, salivary cortisol levels appear to be unaffected by levodopa or dopamine agonist drug treatments ( 283 ), and do not correlate with duration of the disease and motor symptoms ( 282 ).…”

Section: Depression In Parkinson’s Diseasementioning

confidence: 99%

“…It is important to note that cortisol concentrations measured from saliva samples do not reflect any signs of pathology ( 282 ) and this should be a key consideration in the design of future clinical studies. While the inconsistencies between previous plasma profiling studies could be attributed to age, progression of disease or drug treatment, salivary cortisol levels appear to be unaffected by levodopa or dopamine agonist drug treatments ( 283 ), and do not correlate with duration of the disease and motor symptoms ( 282 ). Interestingly, one study reported that salivary cortisol levels could predict which PD patients were more likely to engage in risky behavior ( 284 ) and this could be an important consideration in the context of cognitive deficits or suicide ideation.…”

Section: Depression In Parkinson’s Diseasementioning

confidence: 99%

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Is Dysregulation of the HPA-Axis a Core Pathophysiology Mediating Co-Morbid Depression in Neurodegenerative Diseases?

2015

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There is increasing evidence of prodromal manifestation of neuropsychiatric symptoms in a variety of neurodegenerative diseases such as Parkinson’s disease (PD) and Huntington’s disease (HD). These affective symptoms may be observed many years before the core diagnostic symptoms of the neurological condition. It is becoming more apparent that depression is a significant modifying factor of the trajectory of disease progression and even treatment outcomes. It is therefore crucial that we understand the potential pathophysiologies related to the primary condition, which could contribute to the development of depression. The hypothalamic–pituitary–adrenal (HPA)-axis is a key neuroendocrine signaling system involved in physiological homeostasis and stress response. Disturbances of this system lead to severe hormonal imbalances, and the majority of such patients also present with behavioral deficits and/or mood disorders. Dysregulation of the HPA-axis is also strongly implicated in the pathology of major depressive disorder. Consistent with this, antidepressant drugs, such as the selective serotonin reuptake inhibitors have been shown to alter HPA-axis activity. In this review, we will summarize the current state of knowledge regarding HPA-axis pathology in Alzheimer’s, PD and HD, differentiating between prodromal and later stages of disease progression when evidence is available. Both clinical and preclinical evidence will be examined, but we highlight animal model studies as being particularly useful for uncovering novel mechanisms of pathology related to co-morbid mood disorders. Finally, we purpose utilizing the preclinical evidence to better inform prospective, intervention studies.

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Section: Depression In Parkinson’s Diseasementioning

confidence: 99%

Section: Depression In Parkinson’s Diseasementioning

confidence: 99%

Is Dysregulation of the HPA-Axis a Core Pathophysiology Mediating Co-Morbid Depression in Neurodegenerative Diseases?

2015

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“…Parkinson's disease (PD) is a multifactorial complex disorder associated with motor signs as well as diverse nonmotor symptoms such as circadian disruption, depression, and cognitive decline. Dysregulation of the hypothalamic‐pituitary‐adrenal (HPA) axis, evidenced by hypersecretion of cortisol, is implicated in such nonmotor symptoms, and elevated levels of cortisol have been documented in PD, especially in the morning . Participation in physical activity may reduce the risk and rate of progression of PD, and endurance exercise may reduce the rate at which the signs of PD progress .…”

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confidence: 99%

Endurance exercise reduces cortisol in Parkinson's disease with mild cognitive impairment

et al. 2019

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“…Moreover, a decrease in the amplitude and total amount of melatonin and cortisol secretion has been observed [ 29 , 30 ]. In another study, the pattern of cortisol secretion was also blunted, but total cortisol concentrations were increased in PD subjects compared to healthy controls [ 31 ]. These changes in melatonin and cortisol secretion patterns have also been reported in non-PD subjects with a depressive disorder or insomnia [ 32 – 34 ].…”

Section: Introductionmentioning

confidence: 99%

A double-blind randomized controlled trial to assess the effect of bright light therapy on depression in patients with Parkinson’s disease

et al. 2016

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BackgroundA disturbed circadian rhythm seems to be a causal factor in the occurrence of depressive disorders in patients with Parkinson’s disease (PD). The circadian rhythm can be restored with light. Therefore, Bright Light Therapy (BLT) might be a new treatment option for depression in PD patients.Methods/designIn this double-blind controlled trial, 84 subjects with idiopathic PD are randomized to either BLT or a control light condition. The BLT condition emits white light with an intensity of 10,000 Lux, while the control device emits dim white light of 200 Lux, which is presumed to be too low to influence the circadian rhythm. Subjects receive 30 min of home treatment twice daily for three months. Timing of treatment is based on the individual chronotype. After finishing treatment, subjects enter a follow-up period of six months. The primary outcome of the study is the severity of depressive symptoms, as measured with the Hamilton Depression Rating Scale. Secondary outcomes are alternative depression measures, objective and subjective sleep measures, and salivary melatonin and cortisol concentrations. For exploratory purposes, we also assess the effects on motor symptoms, global cognitive function, comorbid psychiatric disorders, quality of life and caregiver burden. Data will be analyzed using a linear mixed models analysis.DiscussionPerforming a placebo-controlled trial on the effects of BLT in PD patients is challenging, as the appearance of the light may provide clues on the treatment condition. Moreover, fixed treatment times lead to an improved sleep-wake rhythm, which also influences the circadian system. With our study design, we do not compare BLT to placebo treatment, i.e. an ineffective control treatment. Rather, we compare structuring of the sleep-wake cycle in both conditions with additional BLT in the experimental condition, and additional dim light in the control condition. Participants are not informed about the exact details of the two light devices and the expected therapeutic effect, and expectancies are rated prior to the start of treatment. Ideally, the design of a future study on BLT should include two extra treatment arms where BLT and control light are administered at random times.Trial registrationThis trial was registered on ClinicalTrials.gov on May 17th 2012 (ClinicalTrials.gov Identifier: NCT01604876).

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Diurnal salivary cortisol concentrations in Parkinson’s disease: increased total secretion and morning cortisol concentrations

Cited by 18 publications

References 37 publications

Is Dysregulation of the HPA-Axis a Core Pathophysiology Mediating Co-Morbid Depression in Neurodegenerative Diseases?

Is Dysregulation of the HPA-Axis a Core Pathophysiology Mediating Co-Morbid Depression in Neurodegenerative Diseases?

Endurance exercise reduces cortisol in Parkinson's disease with mild cognitive impairment

A double-blind randomized controlled trial to assess the effect of bright light therapy on depression in patients with Parkinson’s disease

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