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Relevant bibliographies by topics / Melatonin – Pathophysiology

Academic literature on the topic 'Melatonin – Pathophysiology'

Author: Grafiati

Published: 10 December 2022

Last updated: 29 January 2023

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Journal articles on the topic "Melatonin – Pathophysiology"

1

Hardeland, Rüdiger. "Neurobiology, Pathophysiology, and Treatment of Melatonin Deficiency and Dysfunction." Scientific World Journal 2012 (2012): 1–18. http://dx.doi.org/10.1100/2012/640389.

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Melatonin is a highly pleiotropic signaling molecule, which is released as a hormone of the pineal gland predominantly during night. Melatonin secretion decreases during aging. Reduced melatonin levels are also observed in various diseases, such as types of dementia, some mood disorders, severe pain, cancer, and diabetes type 2. Melatonin dysfunction is frequently related to deviations in amplitudes, phasing, and coupling of circadian rhythms. Gene polymorphisms of melatonin receptors and circadian oscillator proteins bear risks for several of the diseases mentioned. A common symptom of insufficient melatonin signaling is sleep disturbances. It is necessary to distinguish between symptoms that are curable by short melatonergic actions and others that require extended actions during night. Melatonin immediate release is already effective, at moderate doses, for reducing difficulties of falling asleep or improving symptoms associated with poorly coupled circadian rhythms, including seasonal affective and bipolar disorders. For purposes of a replacement therapy based on longer-lasting melatonergic actions, melatonin prolonged release and synthetic agonists have been developed. Therapies with melatonin or synthetic melatonergic drugs have to consider that these agents do not only act on the SCN, but also on numerous organs and cells in which melatonin receptors are also expressed.

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2

Konenkov, Vladimir Iosifovich, Vadim Valerievich Klimontov, Svetlana Viktorovna Michurina, M. A. Prudnikova, and I. Ju Ishenko. "Melatonin and diabetes: from pathophysiology to the treatment perspectives." Diabetes mellitus 16, no. 2 (June 15, 2013): 11–16. http://dx.doi.org/10.14341/2072-0351-3751.

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Pineal hormone melatonin synchronizes insulin secretion and glucose homeostasis with solar periods. Misalliance between melatonin-mediated circadian rhythms and insulin secretion characterizes diabetes mellitus type 1 (T1DM) and type 2 (T2DM). Insulin deficiency in T1DM is accompanied by increased melatonin production. Conversely, T2DM is characterized by diminished melatonin secretion. In genome-wide association studies the variants of melatonin receptor MT2 gene (rs1387153 and rs10830963) were associated with fasting glucose, beta-cell function and T2DM. In experimental models of diabetes melatonin enhanced beta-cell proliferation and neogenesis, improved insulin resistance and alleviated oxidative stress in retina and kidneys. However, further investigation is required to assess the therapeutic value of melatonin in diabetic patients.

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3

Maltsev, S. V., and L. A. Itkina. "Physiology and pathophysiology of melatonin." Kazan medical journal 80, no. 5 (September 15, 1999): 390–93. http://dx.doi.org/10.17816/kazmj70226.

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Studies devoted to the role of biogenic monoamines and peptide hormones in the formation of physiological and pathophysiological reactions have attracted particular attention in recent years. At the same time, the important role of the cells producing these substances, united by Peasse into a single functionally active peripheral neuroendocrine system (APU D-system), is emphasized.

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4

Lee, Jung Goo, Young Sup Woo, Sung Woo Park, Dae-Hyun Seog, Mi Kyoung Seo, and Won-Myong Bahk. "The Neuroprotective Effects of Melatonin: Possible Role in the Pathophysiology of Neuropsychiatric Disease." Brain Sciences 9, no. 10 (October 21, 2019): 285. http://dx.doi.org/10.3390/brainsci9100285.

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Melatonin is a hormone that is secreted by the pineal gland. To date, melatonin is known to regulate the sleep cycle by controlling the circadian rhythm. However, recent advances in neuroscience and molecular biology have led to the discovery of new actions and effects of melatonin. In recent studies, melatonin was shown to have antioxidant activity and, possibly, to affect the development of Alzheimer’s disease (AD). In addition, melatonin has neuroprotective effects and affects neuroplasticity, thus indicating potential antidepressant properties. In the present review, the new functions of melatonin are summarized and a therapeutic target for the development of new drugs based on the mechanism of action of melatonin is proposed.

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5

Peres, MFP. "Melatonin, the Pineal Gland and their Implications for Headache Disorders." Cephalalgia 25, no. 6 (June 2005): 403–11. http://dx.doi.org/10.1111/j.1468-2982.2005.00889.x.

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There is now evidence that melatonin may have a role in the biological regulation of circadian rhythms, sleep, mood, and ageing. Altered melatonin levels in cluster headache and migraine have been documented. Melatonin mechanisms are related to headache pathophysiology in many ways, including its anti-inflammatory effect, toxic free radical scavenging, reduction of proinflammatory cytokine up-regulation, nitric oxide synthase activity and dopamine release inhibition, membrane stabilization, GABA and opioid analgesia potentiation, glutamate neurotoxicity protection, neurovascular regulation, serotonin modulation, and the similarity of chemical structure to that of indomethacin. Treatment of headache disorders with melatonin and other chronobiotic agents is promising. A doubleblind, placebo-controlled trial shows melatonin is effective in cluster headache prevention, other studies also show benefit in other disorders. Melatonin plays an important role in headache disorders, offering new avenues for studying their pathophysiology and treatment.

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6

Reiter, Russel J. "Melatonin and the pathophysiology of cellular membranes." MARMARA PHARMACEUTCAL JOURNAL 1, no. 14 (January 1, 2010): 1–9. http://dx.doi.org/10.12991/201014457.

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7

Claustrat, Bruno, Jocelyne Brun, and Guy Chazot. "The basic physiology and pathophysiology of melatonin." Sleep Medicine Reviews 9, no. 1 (February 2005): 11–24. http://dx.doi.org/10.1016/j.smrv.2004.08.001.

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8

Anderson, George, Moses Rodriguez, and Russel J. Reiter. "Multiple Sclerosis: Melatonin, Orexin, and Ceramide Interact with Platelet Activation Coagulation Factors and Gut-Microbiome-Derived Butyrate in the Circadian Dysregulation of Mitochondria in Glia and Immune Cells." International Journal of Molecular Sciences 20, no. 21 (November 5, 2019): 5500. http://dx.doi.org/10.3390/ijms20215500.

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Recent data highlight the important roles of the gut microbiome, gut permeability, and alterations in mitochondria functioning in the pathophysiology of multiple sclerosis (MS). This article reviews such data, indicating two important aspects of alterations in the gut in the modulation of mitochondria: (1) Gut permeability increases toll-like receptor (TLR) activators, viz circulating lipopolysaccharide (LPS), and exosomal high-mobility group box (HMGB)1. LPS and HMGB1 increase inducible nitric oxide synthase and superoxide, leading to peroxynitrite-driven acidic sphingomyelinase and ceramide. Ceramide is a major driver of MS pathophysiology via its impacts on glia mitochondria functioning; (2) Gut dysbiosis lowers production of the short-chain fatty acid, butyrate. Butyrate is a significant positive regulator of mitochondrial function, as well as suppressing the levels and effects of ceramide. Ceramide acts to suppress the circadian optimizers of mitochondria functioning, viz daytime orexin and night-time melatonin. Orexin, melatonin, and butyrate increase mitochondria oxidative phosphorylation partly via the disinhibition of the pyruvate dehydrogenase complex, leading to an increase in acetyl-coenzyme A (CoA). Acetyl-CoA is a necessary co-substrate for activation of the mitochondria melatonergic pathway, allowing melatonin to optimize mitochondrial function. Data would indicate that gut-driven alterations in ceramide and mitochondrial function, particularly in glia and immune cells, underpin MS pathophysiology. Aryl hydrocarbon receptor (AhR) activators, such as stress-induced kynurenine and air pollutants, may interact with the mitochondrial melatonergic pathway via AhR-induced cytochrome P450 (CYP)1b1, which backward converts melatonin to N-acetylserotonin (NAS). The loss of mitochnodria melatonin coupled with increased NAS has implications for altered mitochondrial function in many cell types that are relevant to MS pathophysiology. NAS is increased in secondary progressive MS, indicating a role for changes in the mitochondria melatonergic pathway in the progression of MS symptomatology. This provides a framework for the integration of diverse bodies of data on MS pathophysiology, with a number of readily applicable treatment interventions, including the utilization of sodium butyrate.

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9

Mondes, Pedro Henrique de Lima, and Eduardo Koji Tamura. "Melatonina em Animais de Companhia: uma Revisão de Literatura." Ensaios e Ciência C Biológicas Agrárias e da Saúde 25, no. 5-esp (March 14, 2022): 671–81. http://dx.doi.org/10.17921/1415-6938.2021v25n5-espp671-681.

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A melatonina, N-acetil-5-metoxi-triptamina, é uma indolamina que possui diversas ações no organismo, desde regulação de ritmos circadianos, modulação do sistema imune, indutor do sono em determinas espécies e até eliminação de radicais livres. O objetivo desta revisão foi descrever o histórico, a síntese, os mecanismos de ação e os efeitos da melatonina, além de descrever trabalhos que utilizaram a melatonina em patologias associadas aos animais domésticos, em especial, nos cães e nos gatos. Esta revisão pode ser classificada como integrativa, com metodologia que consistiu em selecionar artigos das plataformas online como PubMed e Google Acadêmico, com a combinação de palavras-chave como “melatonin”, “dog”, “cat”, “circadian”, “rhythm”, “mammals”, desde que investigassem o envolvimento da indolamina na fisiopatologia de animais de companhia, ou que utilizassem a melatonina como método terapêutico no campo da Medicina Veterinária. Os artigos escolhidos dataram de 1958 até 2020. Os resultados demonstraram efeitos diversos, em várias áreas de especializações da veterinária, entre essas, oncologia, oftalmologia, anestesiologia, reprodução, endocrinologia, neurologia, dermatologia e gastroenterologia. Apesar dos resultados obtidos, a melatonina ainda é pouco estudada em trabalhos clínicos e científicos veterinários e, por isso, necessita de mais investigação, uma vez que possui potencial terapêutico em muitas das enfermidades que acometem animais de companhia. Palavras-chave: Glândula Pineal. Medicina Veterinária. Cães. Gatos. Abstract Melatonin, N-acetyl-5-methoxy-tryptamine, is an indolamine that has various effects in the organism, from regulation of circadian rhythms to immune system modulation, sleep induction in some species and to scavenger of free radicals. This review aimed to described the history, action mechanisms and melatonin effects, in addition to, also describe studies focusing in therapeutic use of melatonin in pathologies associated with companion animals, specially dogs and cats. This review can be classified as integrative, with a methodology consisting of selected articles from online platforms, PubMed and Google Scholar, using the combination of keywords such as “melatonin”, “dog”, “cat”, “circadian”, “rhythm”, “mammals”, since they investigate the indolamine involvement in the companion animals pathophysiology, or that use melatonin as a therapeutic method in the Veterinary Medicine field. The selected articles were from 1958 to 2020. The results demonstrated different effects in some veterinary specialization areas, including oncology, ophthalmology, anesthesiology, reproduction, endocrinology, neurology, dermatology and gastroenterology. Despite the results obtained, melatonin is still poorly studied in clinical and scientific veterinary and, therefore, needs further investigation, since it has therapeutic potential in many diseases that affect companion animals. Keywords: Pineal Gland. Veterinary Medicine. Dogs. Cats.

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10

Mondes, Pedro Henrique de Lima, and Eduardo Koji Tamura. "Melatonina em Animais de Companhia: uma Revisão de Literatura." Ensaios e Ciência C Biológicas Agrárias e da Saúde 25, no. 5-esp. (March 14, 2022): 671–81. http://dx.doi.org/10.17921/1415-6938.2021v25n5-esp.p671-681.

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Abstract:

A melatonina, N-acetil-5-metoxi-triptamina, é uma indolamina que possui diversas ações no organismo, desde regulação de ritmos circadianos, modulação do sistema imune, indutor do sono em determinas espécies e até eliminação de radicais livres. O objetivo desta revisão foi descrever o histórico, a síntese, os mecanismos de ação e os efeitos da melatonina, além de descrever trabalhos que utilizaram a melatonina em patologias associadas aos animais domésticos, em especial, nos cães e nos gatos. Esta revisão pode ser classificada como integrativa, com metodologia que consistiu em selecionar artigos das plataformas online como PubMed e Google Acadêmico, com a combinação de palavras-chave como “melatonin”, “dog”, “cat”, “circadian”, “rhythm”, “mammals”, desde que investigassem o envolvimento da indolamina na fisiopatologia de animais de companhia, ou que utilizassem a melatonina como método terapêutico no campo da Medicina Veterinária. Os artigos escolhidos dataram de 1958 até 2020. Os resultados demonstraram efeitos diversos, em várias áreas de especializações da veterinária, entre essas, oncologia, oftalmologia, anestesiologia, reprodução, endocrinologia, neurologia, dermatologia e gastroenterologia. Apesar dos resultados obtidos, a melatonina ainda é pouco estudada em trabalhos clínicos e científicos veterinários e, por isso, necessita de mais investigação, uma vez que possui potencial terapêutico em muitas das enfermidades que acometem animais de companhia. Palavras-chave: Glândula Pineal. Medicina Veterinária. Cães. Gatos. Abstract Melatonin, N-acetyl-5-methoxy-tryptamine, is an indolamine that has various effects in the organism, from regulation of circadian rhythms to immune system modulation, sleep induction in some species and to scavenger of free radicals. This review aimed to described the history, action mechanisms and melatonin effects, in addition to, also describe studies focusing in therapeutic use of melatonin in pathologies associated with companion animals, specially dogs and cats. This review can be classified as integrative, with a methodology consisting of selected articles from online platforms, PubMed and Google Scholar, using the combination of keywords such as “melatonin”, “dog”, “cat”, “circadian”, “rhythm”, “mammals”, since they investigate the indolamine involvement in the companion animals pathophysiology, or that use melatonin as a therapeutic method in the Veterinary Medicine field. The selected articles were from 1958 to 2020. The results demonstrated different effects in some veterinary specialization areas, including oncology, ophthalmology, anesthesiology, reproduction, endocrinology, neurology, dermatology and gastroenterology. Despite the results obtained, melatonin is still poorly studied in clinical and scientific veterinary and, therefore, needs further investigation, since it has therapeutic potential in many diseases that affect companion animals. Keywords: Pineal Gland. Veterinary Medicine. Dogs. Cats.

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Books on the topic "Melatonin – Pathophysiology"

1

P, Trentini G., De Gaetani C, Pévet P, and European Pineal Study Group. Colloquium, eds. Fundamentals and clinics in pineal research. New York: Raven Press, 1987.

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2

Walter, Pierpaoli, Regelson William, and Fabris N, eds. The aging clock: The pineal gland and other pacemakers in the progression of aging and carcinogenesis : Third Stromboli Conference on Aging and Cancer. New York, N.Y: New York Academy of Sciences, 1994.

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3

1951-, Stevens Richard G., Wilson Bary W. 1945-, and Anderson Larry E. 1943-, eds. The melatonin hypothesis: Breast cancer and use of electric power. Columbus, OH: Battelle Press, 1997.

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(Editor), Richard G. Stevens, Bary W. Wilson (Editor), and Larry E. Anderson (Editor), eds. The Melatonin Hypothesis: Breast Cancer and Use of Electric Power. Battelle Press, 1997.

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Book chapters on the topic "Melatonin – Pathophysiology"

1

Anderson, George, and Michael Maes. "Melatonin in the Etiology, Pathophysiology, and Management of Schizophrenia." In Melatonin and Melatonergic Drugs in Clinical Practice, 307–20. New Delhi: Springer India, 2013. http://dx.doi.org/10.1007/978-81-322-0825-9_22.

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2

Piccirillo, Jay F. "Melatonin." In Tinnitus: Pathophysiology and Treatment, 331–33. Elsevier, 2007. http://dx.doi.org/10.1016/s0079-6123(07)66030-0.

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3

Gupta, Derek. "The Role of Melatonin in Human Pathophysiology." In Melatonin, 417–45. CRC Press, 2020. http://dx.doi.org/10.1201/9781003068570-16.

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4

Aulinas, Anna, Cristina Colom, and Susan M. Webb. "Pineal physiology and pathophysiology, including pineal tumours." In Oxford Textbook of Endocrinology and Diabetes, 267–72. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.2222.

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The pineal gland is innervated mainly by sympathetic nerve fibres that inform the gland of the prevailing light-dark cycle and acts as a neuroendocrine transducer. The gland is located behind the third ventricle in the centre of the brain and is a highly vascular organ formed by neuroglial cells and parenchymal cells or pinealocytes. The latter synthesize melatonin as well as other indoleamines and peptides. The main pineal hormone melatonin (N-acetyl-5-methoxytryp-tamine) exhibits an endogenous circadian rhythm, reflecting signals originating in the suprachiasmatic nucleus; environmental lighting entrains the rhythm, by altering its timing. Independently of sleep, pineal melatonin is inhibited by light and stimulated during darkness, thanks to the neural input by a multisynaptic pathway that connects the retina, through the suprachiasmatic nucleus of the hypothalamus, preganglionic neurons in the upper thoracic spinal cord and postganglionic sympathetic fibres from the superior cervical ganglia, with the pineal gland. Melatonin deficiency may produce sleeping disorders, behavioural problems, or be associated with precocious or delayed puberty in children, while chronically elevated melatonin has been observed in some cases of hypogonadotropic hypogonadism (1, 2).

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Webb, Susan M., Anna Aulinas, Cristina Colom, and María-José Barahona. "Pineal Physiology and Pathophysiology, Including Pineal Tumours." In Oxford Textbook of Endocrinology and Diabetes 3e, edited by John A. H. Wass, Wiebke Arlt, and Robert K. Semple, 312–20. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198870197.003.0036.

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Pineal physiology and tumours are briefly summarized in this chapter. The main pineal hormone melatonin is secreted at night and entrains endogenous rhythms to the environment. Melatonin deficiency has been associated to sleeping disorders, behavioural problems, and abnormal puberty, while its excess has been described in hypogonadotropic hypogonadism. Outcome after diagnosis of a pineal tumour have improved in the last decades after better understanding of the natural history of these tumours, neurosurgical experience, use of chemotherapy, and current irradiation techniques. The low prevalence of these pineal tumours has prevented any large prospective multicentre international studies aimed at identifying optimal management. The most recent World Health Organization (WHO) classification of central nervous system tumours published in 2016, defines molecular parameters as well as histology to classify these tumour entities, formulating a molecular diagnosis for these tumours.

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6

Gray, Weili. "Sleep Health and Sleep Disorders." In Integrative Neurology, 283–326. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780190051617.003.0011.

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This chapter reviews the architecture and functions of sleep, how to interview patients on their sleep histories, how to evaluate for sleep disorders, commonly encountered sleep disorders and their pathophysiology, and the conventional and integrative therapies for each. The evaluation process includes a conventional sleep study as well as addressing vitamin D, B, and magnesium status. Sleep disorders discussed in this chapter are obstructive sleep apnea, insomnia, restless legs syndrome, periodic limb movement disorder, rapid-eye-movement behavior disorder, circadian rhythm disorders, and narcolepsy and other central hypersomnias. The role of conventional tools and times when alternative and complementary therapies may be considered are discussed in detail. Treatment covered include continuous positive airway pressure, oral appliance, myofunctional therapy, cognitive-behavioral therapy for insomnia, physical modalities, acupuncture, light therapy, melatonin, nutraceuticals, and other supplements that aid with sleep and daytime symptoms.

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Feemster, John C., and Erik K. St Louis. "Chorea, Ataxia, and Disturbed Sleep." In Mayo Clinic Cases in Neuroimmunology, edited by Andrew McKeon, B. Mark Keegan, and W. Oliver Tobin, 108–10. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780197583425.003.0033.

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A 72-year-old man sought care for predominant choreiform movements, mild gait ataxia, urinary dysfunction, and abnormal nocturnal behaviors. Choreiform movements were nearly constant while awake, vanished during sleep, and predominantly involved his lower extremities and trunk. He also had urinary dysfunction, with urinary hesitancy and frequency. Sleep-related behaviors included sleep talking, sleep singing, sudden single-limb jerking movements, and complex hand movements. He also had daytime sleepiness. On neurologic examination, abnormal findings included postural instability at baseline with eyes open and a slightly wide-based tentative gait and inability to execute tandem walking. He had intermittent choreiform movements of the legs and the left shoulder. He also had occasional repetitive, periodic, voluntary-appearing, triple flexion–type movements of both legs. Overnight polysomnography was ordered to evaluate nocturnal movements. Polysomnography revealed rapid periodic leg movements of sleep and rapid eye movement sleep without atonia. Sleep architecture was mildly deranged, with electroencephalographic alpha intrusion throughout nonrapid eye movement sleep, as well as absent slow-wave sleep. Ferritin level was suboptimal. Evaluation of serum for autoimmune encephalitis demonstrated IgLON family member 5 antibody positivity by tissue immunofluorescence assay, confirmed by cell-based assay. The patient was diagnosed with IgLON family member 5 autoimmune encephalitis and symptomatic rapid eye movement sleep behavior disorder. The patient was instructed to maintain a safe sleep environment at home and to begin taking melatonin at bedtime. A therapeutic trial of intravenous methylprednisolone, together with mycophenolate mofetil, was followed by improvement in memory, confusion, and hallucinations, waking involuntary movements, bladder dysfunction, and sleep quality. Rapid eye movement sleep behavior disorder is a parasomnia characterized by rapid eye movement sleep without atonia, the loss or dysregulation of normal rapid eye movement sleep atonia, which is its pathophysiologic signature, and which is permissive for dream enactment behaviors during rapid eye movement sleep.

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