TY - JOUR
T1 - Impact of Sleep Deprivation on Major Neuroinflammatory Signal Transduction Pathways
AU - Mahalakshmi, Arehally M.
AU - Lokesh, Prithvi
AU - Hediyal, Tousif Ahmed
AU - Kalyan, Manjunath
AU - Vichitra, Chandrasekaran
AU - Essa, Musthafa Mohamed
AU - Qoronfleh, M. Walid
AU - Pandi-Perumal, Seithikurippu R.
AU - Chidambaram, Saravana Babu
N1 - Funding Information:
The authors thank their respective institutions for providing the required infrastructure to produce this manuscript.
Publisher Copyright:
© 2022, The Author(s), under exclusive licence to Springer Nature Singapore Pte Ltd.
PY - 2022/5/20
Y1 - 2022/5/20
N2 - Sleep deprivation (SD) is emulating an epidemic imparting detrimental effects ranging from immediate repercussions like vehicle accidents to very serious neurological disorders. All age groups are vulnerable to SD either because of lifestyle or illness. This imposes a significant burden on public health and safety. SD triggers an array of inflammatory responses, and neuroinflammation is one of the most common complications. Changes in circulation levels of pro- and anti-inflammatory cytokines caused by SD are associated with higher and lower levels of inflammation, respectively. SD-induced astrogliosis, microgliosis, impaired glymphatic clearance, BBB disruption, and release of inflammatory cytokines are the main sources of neuroinflammation. This review addresses the clinical and experimental SD and the associated activation of neuroinflammatory signaling via NF-κB, TNF-α, CREB, TLR, Nrf2, JAK-STAT, MAPK, and mTOR proteins. Major neurodegenerative disorders (e.g., Alzheimer's disease (AD), Parkinson's disease (PD), and Amyotrophic lateral sclerosis (ALS) all have these signaling molecules as crucial participants in their etiology. Hence, SD has a strong association with the initiation and progression of neurodegenerative diseases. Further research in this area is warranted to understand the role of the activated neuroinflammatory pathways in the initiation, progression, and manifestations of neurological disorders.
AB - Sleep deprivation (SD) is emulating an epidemic imparting detrimental effects ranging from immediate repercussions like vehicle accidents to very serious neurological disorders. All age groups are vulnerable to SD either because of lifestyle or illness. This imposes a significant burden on public health and safety. SD triggers an array of inflammatory responses, and neuroinflammation is one of the most common complications. Changes in circulation levels of pro- and anti-inflammatory cytokines caused by SD are associated with higher and lower levels of inflammation, respectively. SD-induced astrogliosis, microgliosis, impaired glymphatic clearance, BBB disruption, and release of inflammatory cytokines are the main sources of neuroinflammation. This review addresses the clinical and experimental SD and the associated activation of neuroinflammatory signaling via NF-κB, TNF-α, CREB, TLR, Nrf2, JAK-STAT, MAPK, and mTOR proteins. Major neurodegenerative disorders (e.g., Alzheimer's disease (AD), Parkinson's disease (PD), and Amyotrophic lateral sclerosis (ALS) all have these signaling molecules as crucial participants in their etiology. Hence, SD has a strong association with the initiation and progression of neurodegenerative diseases. Further research in this area is warranted to understand the role of the activated neuroinflammatory pathways in the initiation, progression, and manifestations of neurological disorders.
KW - Neurodegenerative disease
KW - Neuroinflammation
KW - Oxidative stress
KW - Signaling pathways
KW - Sleep deprivation
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UR - https://www.mendeley.com/catalogue/9f485c64-e884-3257-bb3f-d012405b10c3/
U2 - 10.1007/s41782-022-00203-6
DO - 10.1007/s41782-022-00203-6
M3 - Article
AN - SCOPUS:85130275606
SN - 2510-2265
VL - 6
SP - 101
EP - 114
JO - Sleep and Vigilance
JF - Sleep and Vigilance
IS - 1
ER -
