Deacceleration of Brain Aging by Melatonin

Hardeland, Rüdiger

doi:10.1007/978-3-319-33486-8_18

Cited by 4 publications

(2 citation statements)

References 183 publications

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“…The actions of melatonin on microglia cannot be seen independently of other cells in the CNS. The interplay of neurons, astrocytes, and microglia has been repeatedly addressed in articles on neuroprotection and neurodegeneration as well [ 76 , 77 , 78 , 79 , 80 ], including papers that have focused on melatonin [ 2 , 21 , 81 , 82 ]. The multidirectionality of these connections is astonishingly pronounced and important.…”

Section: Melatonin Influences Glial and Glial-neuronal Interactionsmentioning

confidence: 99%

Melatonin and Microglia

Hardeland

2021

IJMS

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Melatonin interacts in multiple ways with microglia, both directly and, via routes of crosstalk with astrocytes and neurons, indirectly. These effects of melatonin are of relevance in terms of antioxidative protection, not only concerning free-radical detoxification, but also in prevention of processes that cause, promote, or propagate oxidative stress and neurodegeneration, such as overexcitation, toxicological insults, viral and bacterial infections, and sterile inflammation of different grades. The immunological interplay in the CNS, with microglia playing a central role, is of high complexity and includes signaling toward endothelial cells and other leukocytes by cytokines, chemokines, nitric oxide, and eikosanoids. Melatonin interferes with these processes in multiple signaling routes and steps. In addition to canonical signal transduction by MT1 and MT2 melatonin receptors, secondary and tertiary signaling is of relevance and has to be considered, e.g., via the upregulation of sirtuins and the modulation of pro- and anti-inflammatory microRNAs. Many details concerning the modulation of macrophage functionality by melatonin are obviously also applicable to microglial cells. Of particular interest is the polarization toward M2 subtypes instead of M1, i.e., in favor of being anti-inflammatory at the expense of proinflammatory activities, which is well-documented in macrophages but also applies to microglia.

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Section: Melatonin Influences Glial and Glial-neuronal Interactionsmentioning

confidence: 99%

Melatonin and Microglia

Hardeland

2021

IJMS

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“…The anti-inflammatory actions of melatonin are also, in part, associated with mitochondrial functions, as recently outlined in the context of COVID-19 (1). The protective mechanisms by which melatonin acts, especially under conditions of high-grade inflammation and in aging, have been repeatedly reviewed (3,4,90). A particular aspect that has emerged during the last years concerns the involvement SIRT1 in melatonin's anti-inflammatory actions (3,4,(27)(28)(29)(30).…”

Section: The Relevance Of Anti-inflammatory and Antioxidant Treatmentmentioning

confidence: 99%

Protection by melatonin in respiratory diseases: valuable information for the treatment of COVID-19

Hardeland

Tan²

2020

Melatonin Res.

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High mortality rates in severe progression of COVID-19 are predominantly caused by pulmonary failure due to high-grade airway inflammation. As investigations on the efficacy of melatonin in this disease are still in their beginning, it may be worth-while to recall the body of evidence on protective effects in other respiratory dysfunctions, which have been studied pre-clinically and clinically. In various diseases and corresponding animal models, melatonin has been shown to be protective, mainly because of its anti-inflammatory and antioxidant properties. This was documented in pathologies as different as allergic airway inflammation, toxicologically or radiation-induced acute lung injury, respiratory disorders such as COPD, obstructive sleep apnea, neonatal respiratory distress syndrome, bronchopulmonary dysplasia and asphyxia, impaired respiration in sepsis, idiopathic pulmonary fibrosis, and pulmonary hypertension. The prevailing outcome has been protection or amelioration by melatonin, in conjunction with reduced expression and release of proinflammatory cytokines, such as IL-1β, IL-2, IL-6, IL-8, and TNFα, which was often explained by interference with toll-like receptors, inhibition of NLRP3 inflammasome activation and suppression of NF-κB signaling. In several studies, these beneficial effects were partially related to the upregulation of sirtuin-1 (SIRT1) by melatonin. The body of knowledge on melatonin’s efficacy in respiratory diseases is encouraging for the use of this powerful agent in COVID-19.

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Hormones in Clock Regulation During Ageing

Jagota

Thummadi

2017

Healthy Ageing and Longevity

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Deacceleration of Brain Aging by Melatonin

Cited by 4 publications

References 183 publications

Melatonin and Microglia

Melatonin and Microglia

Protection by melatonin in respiratory diseases: valuable information for the treatment of COVID-19

Hormones in Clock Regulation During Ageing

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