Decoding the Inter-Relationship between Sleep Disorders and Alzheimer's Disease Pathogenesis
Autor: | Pankaj Kumar Rai, Nitesh Kumar Poddar, Mohammad Amjad Kamal, Zeba Mueed |
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Rok vydání: | 2020 |
Předmět: |
Light therapy
Sleep Wake Disorders Amyloid medicine.medical_treatment Amyloidogenic Proteins tau Proteins Disease Neuroprotection Melatonin Alzheimer Disease Medicine Humans Phosphorylation PI3K/AKT/mTOR pathway Pharmacology Sleep disorder Amyloid beta-Peptides business.industry Mechanism (biology) General Neuroscience Neurofibrillary Tangles medicine.disease business Sleep Neuroscience medicine.drug |
Zdroj: | CNSneurological disorders drug targets. 20(8) |
ISSN: | 1996-3181 |
Popis: | Alzheimer’s Disease (AD), characterized by abnormally phosphorylated tau, Paired Helical Filaments (PHFs), Neurofibrillary Tangles (NFTs), deregulated mammalian Target Of Rapamycin (mTOR), and Aβ deposits, is a multifactorial disease with sleep disorders being one of the causative agents. Therefore, we have reviewed the literature and have tried to decode the existence of positive feedback, reciprocal and a bidirectional relationship allying between sleep disturbances and AD. Much light has been thrown on the role of tau pathology and amyloid pathology in sleep pathology and its association with AD pathology. We have also discussed the role of melatonin in regulating sleep disorders and AD. The neuroprotective effect of melatonin via inhibiting tau hyperphosphorylation and Aβ deposition has also been discussed. Moreover, astrocytes involvement in aggravating AD has also been highlighted in this review. Several therapeutic approaches aimed at improving both sleep disorders and AD have been duly discussed such as administration of antidepressants and antihistamines, immunotherapy, metal chelators, melatonin supplementation, light therapy and physical activity. Despite consistent efforts, the complete etiology concerning sleep disorder and AD is still unclear. Therefore, further research is needed to unravel the mechanism involved and also to develop strategies that may help in obstructing AD in its preclinical stage. |
Databáze: | OpenAIRE |
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