Twenty-Four Hour Cortisol Release Profiles in Patients With Alzheimer's and Parkinson's Disease Compared to Normal Controls: Ultradian Secretory Pulsatility and Diurnal Variation

Hartmann, Andreas; Veldhuis, Johannes D.; Deuschle, Michael; Standhardt, Harald; Heuser, Isabella

doi:10.1016/s0197-4580(97)80309-0

Cited by 276 publications

(200 citation statements)

References 41 publications

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“…Clinical reports of GC hypersecretion in AD patients and in cases of mild cognitive impairment, a condition with a high conversion rate to AD (Hartmann et al, 1997;Weiner et al, 1997;Elgh et al, 2006;Wilson et al, 2007), prompted us to examine how elevated GC secretion, induced by chronic unpredictable stress, influences the pattern of tau phosphorylation in the hippocampus and PFC, brain regions that are established targets of the deleterious morphological and behavioral actions of stress and GC (Sousa et al, 2000;Cerqueira et al, 2007;Schubert et al, 2008;Sotiropoulos et al, 2008a) and among the first to show signs of AD neuropathology (Lace et al, 2009).…”

Section: Resultsmentioning

confidence: 99%

“…This view is supported by reports of hypersecretion of stress hormones [glucocorticoids (GCs)] in AD patients (Hartmann et al, 1997;Weiner et al, 1997;Elgh et al, 2006), and indications that psychological distress may cause mild cognitive impairment (Wilson et al, 2003) and predispose affected individuals to AD (Wilson et al, 2007). Studies in humans and animals demonstrate a robust relationship among elevated GC secretion, cognitive impairment, and neuronal atrophy.…”

Section: Introductionmentioning

confidence: 96%

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Stress Acts Cumulatively To Precipitate Alzheimer's Disease-Like Tau Pathology and Cognitive Deficits

Sotiropoulos

Catania

Pinto³

et al. 2011

J. Neurosci.

214

170

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Stressful life experiences are likely etiological factors in sporadic forms of Alzheimer's disease (AD). Many AD patients hypersecrete glucocorticoids (GCs), and their GC levels correlate with the rate of cognitive impairment and extent of neuronal atrophy. Severity of cognitive deficits in AD correlates strongly with levels of hyperphosphorylated forms of the cytoskeletal protein TAU, an essential mediator of the actions of amyloid ␤ (A␤), another molecule with a key pathogenic role in AD. Our objective was to investigate the sequential interrelationships between these various pathogenic elements, in particular with respect to the mechanisms through which stress might precipitate cognitive decline. We thus examined whether stress, through the mediation of GCs, influences TAU hyperphosphorylation, a critical and early event in the cascade of processes leading to AD pathology. Results from healthy, wild-type, middle-aged rats show that chronic stress and GC induce abnormal hyperphosphorylation of TAU in the hippocampus and prefrontal cortex (PFC), with contemporaneous impairments of hippocampus-and PFC-dependent behaviors. Exogenous GC potentiated the ability of centrally infused A␤ to induce hyperphosphorylation of TAU epitopes associated with AD and cytoplasmic accumulation of TAU, while previous exposure to stress aggravated the biochemical and behavioral effects of GC in A␤-infused animals. Thus, lifetime stress/GC exposure may have a cumulative impact on the onset and progress of AD pathology, with TAU hyperphosphorylation serving to transduce the negative effects of stress and GC on cognition.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 96%

Stress Acts Cumulatively To Precipitate Alzheimer's Disease-Like Tau Pathology and Cognitive Deficits

Sotiropoulos

Catania

Pinto³

et al. 2011

J. Neurosci.

214

170

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“…They found that PD patients secrete significantly more cortisol per burst into plasma and the diurnal mean cortisol secretion rate is significantly higher but tends to be flattened than the age-matched controls. Furthermore, the concomitant L-dopa therapy may not contribute to this endocrine abnormality, as dopamine does not play a major role in modulating the HPA system activity [77]. The hypercortisolism has also been found in patients with earlystage PD.…”

Section: Cortisolmentioning

confidence: 99%

A New Perspective for Parkinson’s Disease: Circadian Rhythm

Wang

et al. 2016

Neurosci. Bull.

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Circadian rhythm is manifested by the behavioral and physiological changes from day to night, which is controlled by the pacemaker and its regulator. The former is located at the suprachiasmatic nuclei (SCN) in the anterior hypothalamus, while the latter is composed of clock genes present in all tissues. Circadian desynchronization influences normal patterns of day-night rhythms such as sleep and alertness cycles, rest and activity cycles. Parkinson's disease (PD) exhibits diurnal fluctuations. Circadian dysfunction has been observed in PD patients and animal models, which may result in negative consequences to the homeostasis and even exacerbate the disease progression. Therefore, circadian therapies, including light stimulation, physical activity, dietary and social schedules, may be helpful for PD patients. However, the cellular and molecular mechanisms that underlie the circadian dysfunction in PD remain elusive. Further research on circadian patterns is needed. This article summarizes the existing research on the circadian rhythms in PD, focusing on the clinical symptom variations, molecular changes, as well as the available treatment options.

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“…In the neuropsychiatric context, neurodegenerative disorders like AD and PD, or depression and post-traumatic stress disorder have been thoroughly studied. Apart from the disturbed circadian pattern (increased waking / morning levels and circadian amplitude) and the increased mean systemic cortisol levels observed in AD (Martignoni et al, 1990;Lei, 2010), analysis of the 24 h ultradian profile of AD (and PD) patients reveals that the hypercortisolemia observed in these subjects results from a raised mass of cortisol secreted per burst compared to healthy age-matched volunteers without any substantial alterations in the cortisol half-life, number of secretory bursts within 24 h, and the mean intersecretory pulse interval (Hartmann et al, 1997). On the contrary, the possible existence of a dysregulated HPA axis in major depression (Pariante and Lightman, 2008) leading to hypercortisolemia, or fibromyalgia and chronic fatigue syndrome (Cleare, 2004;Calis et al, 2004;Wingenfeld et al, 2008) leading to hypocortisolemia, is not accompanied by substantial changes in the ultradian pattern of circulating GCs in the majority of particular subgroup of patients, although further studies are required (Young et al, 2001;Crofford et al, 2004).…”

Section: Altered Hpa Rhythmicity In Stressful Conditions and Human Pamentioning

confidence: 99%

“…Other examples involve the reduction of immune system's sensitivity to GCs' immunosuppressive effects during chronic psychological stress (Miller et al, 2002), or the selective down-regulation of hippocampal GRs under sustained stress in rodents and non-human primates (Brooke et al, 1994) or after the experimental induction of viral encephalitis in rats (Bener et al, 2007). Additionally, GC resistance is thought to contribute to neuropathological mechanisms related to AD (another condition accompanied with an upregulated ultradian pattern) (Hartmann et al, 1997) such as disrupted axonal transport in cortical areas (Dai et al, 2004).…”

Section: How Does Rhythmicity Contribute To the Diverse And Frequentlmentioning

confidence: 99%

Temporal control of glucocorticoid neurodynamics and its relevance for brain homeostasis, neuropathology and glucocorticoid-based therapeutics

Kalafatakis

Russell

Ζάρρος³

et al. 2016

Neuroscience & Biobehavioral Reviews

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Glucocorticoids mediate plethora of actions throughout the human body. Within the brain, they modulate aspects of immune system and neuroinflammatory processes, interfere with cellular metabolism and viability, interact with systems of neurotransmission and regulate neural rhythms. The influence of glucocorticoids on memory and emotional behaviour is well known and there is increasing evidence for their involvement in many neuropsychiatric pathologies. These effects, which at times can be in opposing directions, depend not only on the concentration of glucocorticoids but also the duration of their presence, the temporal relationship between their fluctuations, the co-influence of other stimuli, and the overall state of brain activity. Moreover, they are region-and cell type-specific. The molecular basis of such diversity of effects lies on the orchestration of the spatiotemporal interplay between glucocorticoid-and mineralocorticoid receptors, and is achieved through complex dynamics, mainly mediated via the circadian and ultradian pattern of glucocorticoid secretion. More sophisticated methodologies are therefore required to better approach the study of these hormones and improve the effectiveness of glucocorticoid-based therapeutics.

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Twenty-Four Hour Cortisol Release Profiles in Patients With Alzheimer's and Parkinson's Disease Compared to Normal Controls: Ultradian Secretory Pulsatility and Diurnal Variation

Cited by 276 publications

References 41 publications

Stress Acts Cumulatively To Precipitate Alzheimer's Disease-Like Tau Pathology and Cognitive Deficits

Stress Acts Cumulatively To Precipitate Alzheimer's Disease-Like Tau Pathology and Cognitive Deficits

A New Perspective for Parkinson’s Disease: Circadian Rhythm

Temporal control of glucocorticoid neurodynamics and its relevance for brain homeostasis, neuropathology and glucocorticoid-based therapeutics

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