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2000
Volume 18, Issue 3
  • ISSN: 1574-8863
  • E-ISSN: 2212-3911

Abstract

Background: Alzheimer’s disease (AD) is an age-dependent neurodegenerative disease with progressive cognition and memory loss, insomnia, and other abnormal behavioral changes. Amongst various hypotheses for AD pathophysiology, occupational stress-induced Alzheimer’s has recently been reported in many AD cases. Objective: Studies pertaining to the same suggest that stress leads to insomnia or sleep disruption, which further leads to neuroinflammation due to oxidative stress, both of which are major harbingers of AD. Additionally, overall sleep deficit is associated with progressive cognitive and memory decline, which adds more inconvenience to Alzheimer’s disease. Based on this, any triumphant AD management needs a pharmacological intervention that can not only antagonize the amyloid betainduced neurotoxicity but also correct the sleep-wake cycle disruption. Chronobiotic therapeutics like melatonin offer vital neuroprotective effects by eliciting its action through more than one of the pathologies of AD. This is also bolstered by the finding that endogenous melatonin levels are lower in AD patients. This melatonin replacement therapy can be especially useful in AD treatment, but only in the early phases of the disease and in cases where the melatonin receptors are intact and functioning. Conclusion: To negate such limitations and extend the action and therapeutic efficacy of melatonin- mediated actions towards AD treatment, melatonin analogue like tasimelteon can pose a high therapeutic value in AD treatment superior to that provided by melatonin. This review encapsulates all details about how AD is believed to occur and how current situations influence it, along with how melatonin and tasimelteon act towards treating Alzheimer’s.

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/content/journals/cds/10.2174/1574886317666220517125644
2023-08-01
2025-09-04
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