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Deciphering the Interacting Mechanisms of Circadian Disruption and Alzheimer's Disease

期刊

NEUROCHEMICAL RESEARCH
卷 46, 期 7, 页码 1603-1617

出版社

SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-021-03325-x

关键词

Circadian disruption; Sleep deprivation; Rapid eye movement; Slow-wave sleep; Alzheimer’ s disease; Amyloid beta; Neurofibrillary tangles

资金

  1. Pharmakon Neuroscience Research Network, Dhaka, Bangladesh

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Alzheimer's disease is a crucial factor in progressive dementia, characterized by the accumulation of amyloid beta plaques in the brain. The dysfunction of the circadian system in AD may lead to irregular sleep patterns, which in turn can exacerbate the progression of the disease. Understanding the interaction between circadian disruption and AD pathogenesis is important for earlier detection and potential therapies for dementia.
Alzheimer's disease (AD) is one of the crucial causative factors for progressive dementia. Neuropathologically, AD is characterized by the extracellular accumulation of amyloid beta plaques and intracellular neurofibrillary tangles in cortical and limbic regions of the human brain. The circadian system is one of the many affected physiological processes in AD, the dysfunction of which may reflect in the irregularity of the sleep/wake cycle. The interplay of circadian and sleep disturbances inducing AD progression is bidirectional. Sleep-associated pathological alterations are frequently evident in AD. Understanding the interrelation between circadian disruption and AD may allow for earlier identification of AD pathogenesis as well as better suited approaches and potential therapies to combat dementia. In this article, we examine the existing literature related to the molecular mechanisms of the circadian clock and interacting mechanisms of circadian disruption and AD pathogenesis.

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