The Trajectory of Biomarkers in Symptom Management for Older Adults With Cancer

Payne, Jason

doi:10.1016/j.soncn.2005.10.005

Cited by 12 publications

(4 citation statements)

References 14 publications

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“…In the fetal period, the fetus uses maternal melatonin that crosses the placenta (35), and from birth to a peak around puberty, the melatonin level increases (36) and then declines in middle-aged and elderly individuals (37). As nocturnal melatonin declines in adulthood, its functional effects are gradually impaired.…”

Section: Melatonin During Agingmentioning

confidence: 99%

Effects of Melatonin on Nervous System Aging: Neurogenesis and Neurodegeneration

et al. 2013

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Abstract. Neural aging as a progressive loss of function involves central and peripheral postmitotic neurons and neural stem cells (NSCs). It promotes neurodegeneration, impairs neurogenesis, and can be considered a cause of cognitive impairment and sensory and motor deficits in the elderly. Age-related morphological atrophic changes and cellular alterations are addressed by neural aging mechanisms. Neurogenesis declines during aging through several mechanisms such as an increase in quiescence state, changes in lineage fate, telomerase dysfunction, the failure of the DNA repair system, increased apoptosis, and the impairment of self-renewal. The selfrenewal transcriptional factor Sox2 has been correlated with retrotransposon L1 and certain cellcycle-and epigenetic-related factors, which are sometimes considered age-related factors in NSC aging. As neurogenesis decreases, non-mitotic neurons undergo neurodegeneration by oxidative stress, sirtuin, insulin signaling and mTOR alteration, mitochondrial dysfunction, and protein misfolding and aggregation. As neurodegeneration and impaired neurogenesis promote the nervous system aging process, the identification of neuronal anti-aging is required to raise life expectancy. The role of melatonin in increasing neurogenesis and protecting against neurodegeneration has been investigated. Here, we review nervous system aging that is correlated with mechanisms of neurodegeneration and the impairment of neurogenesis and evaluate the effects of melatonin on these processes.

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Section: Melatonin During Agingmentioning

confidence: 99%

Effects of Melatonin on Nervous System Aging: Neurogenesis and Neurodegeneration

et al. 2013

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“…35,60,71–73 The theoretical underpinning for the proinflammatory cytokine hypothesis, based on the animal model of inflammation-induced sickness behavior, is that dysregulated inflammation and its downstream toxic effects represent a significant biologic basis for subjectively reported CRF and a cluster of other symptoms. 65,66,74 …”

Section: Proposed Mechanisms Of Crf Pathophysiologymentioning

confidence: 99%

Pathophysiology of Cancer-Related Fatigue

Wang¹

2008

Clinical Journal of Oncology Nursing

111

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Cancer-related fatigue (CRF) is influenced and modulated by a number of critical factors, and the mechanism that is both necessary and sufficient to induce development of severe fatigue in patients with cancer has not yet been identified. Specific research efforts on understanding the factors that may contribute to development of CRF have been made, such as studies of the direct effects of tumor burden, the effects of cancer treatment, and other pathophysiological and psychosocial conditions. Compelling new hypotheses regarding the pathophysiology of CRF have been proposed, such as the pro-inflammatory hypothesis, the serotonin hypothesis, the vagal-afferent-activation hypothesis, the anemia hypothesis, and the adenosine triphosphate hypothesis; some of these have been tested in both animal models and humans and some in animals only. Gaining an understanding of the specific mechanisms related to the development of fatigue in patients with cancer and survivors of cancer requires further investigation. Pathophysiological research in CRF could be applied in the clinic to improve diagnosis of CRF and to enable administration of mechanism-driven interventions. A targeted intervention study with CRF as a primary end point would also be useful.

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“…Melatonin levels in individuals increase from birth and peak around puberty [ 15 ]. Its synthesis [ 16 ] and levels decline in middle-aged and most elderly individuals [ 17 ] along with a simultaneous reduction in the urinary excretion of its metabolites [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of Melatonin in Alleviating Alzheimer’s Disease

et al. 2017

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Alzheimer’s disease (AD) is a chronic, progressive and prevalent neurodegenerative disease characterized by the loss of higher cognitive functions and an associated loss of memory. The thus far “incurable” stigma for AD prevails because of variations in the success rates of different treatment protocols in animal and human studies. Among the classical hypotheses explaining AD pathogenesis, the amyloid hypothesis is currently being targeted for drug development. The underlying concept is to prevent the formation of these neurotoxic peptides which play a central role in AD pathology and trigger a multispectral cascade of neurodegenerative processes post-aggregation. This could possibly be achieved by pharmacological inhibition of β- or γ-secretase or stimulating the non-amyloidogenic α-secretase. Melatonin the pineal hormone is a multifunctioning indoleamine. Production of this amphiphilic molecule diminishes with advancing age and this decrease runs parallel with the progression of AD which itself explains the potential benefits of melatonin in line of development and devastating consequences of the disease progression. Our recent studies have revealed a novel mechanism by which melatonin stimulates the nonamyloidogenic processing and inhibits the amyloidogenic processing of β-amyloid precursor protein (βAPP) by stimulating α-secretases and consequently down regulating both β- and γ-secretases at the transcriptional level. In this review, we discuss and evaluate the neuroprotective functions of melatonin in AD pathogenesis, including its role in the classical hypotheses in cellular and animal models and clinical interventions in AD patients, and suggest that with early detection, melatonin treatment is qualified to be an anti-AD therapy.

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The Trajectory of Biomarkers in Symptom Management for Older Adults With Cancer

Cited by 12 publications

References 14 publications

Effects of Melatonin on Nervous System Aging: Neurogenesis and Neurodegeneration

Effects of Melatonin on Nervous System Aging: Neurogenesis and Neurodegeneration

Pathophysiology of Cancer-Related Fatigue

Mechanisms of Melatonin in Alleviating Alzheimer’s Disease

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