Please use this identifier to cite or link to this item: https://doi.org/10.1186/s13024-021-00506-8
Title: The role of inflammasomes in vascular cognitive impairment
Authors: Poh, Luting 
Sim, Wei Liang
Jo, Dong-Gyu
Dinh, Quynh Nhu
Drummond, Grant R
Sobey, Christopher G
Chen, Christopher Li-Hsian 
Lai, Mitchell KP 
Fann, David Y 
Arumugam, Thiruma V 
Keywords: Science & Technology
Life Sciences & Biomedicine
Neurosciences
Neurosciences & Neurology
Inflammasome
Inflammation
Chronic cerebral Hypoperfusion
Vascular cognitive impairment
Vascular dementia
BLOOD-BRAIN-BARRIER
CHRONIC CEREBRAL HYPOPERFUSION
WHITE-MATTER LESIONS
NF-KAPPA-B
SMALL VESSEL DISEASE
ALZHEIMERS-DISEASE
NLRP3 INFLAMMASOME
OXIDATIVE STRESS
AIM2 INFLAMMASOME
NEURONAL DEATH
Issue Date: 9-Jan-2022
Publisher: BMC
Citation: Poh, Luting, Sim, Wei Liang, Jo, Dong-Gyu, Dinh, Quynh Nhu, Drummond, Grant R, Sobey, Christopher G, Chen, Christopher Li-Hsian, Lai, Mitchell KP, Fann, David Y, Arumugam, Thiruma V (2022-01-09). The role of inflammasomes in vascular cognitive impairment. MOLECULAR NEURODEGENERATION 17 (1). ScholarBank@NUS Repository. https://doi.org/10.1186/s13024-021-00506-8
Abstract: There is an increasing prevalence of Vascular Cognitive Impairment (VCI) worldwide, and several studies have suggested that Chronic Cerebral Hypoperfusion (CCH) plays a critical role in disease onset and progression. However, there is a limited understanding of the underlying pathophysiology of VCI, especially in relation to CCH. Neuroinflammation is a significant contributor in the progression of VCI as increased systemic levels of the proinflammatory cytokine interleukin-1β (IL-1β) has been extensively reported in VCI patients. Recently it has been established that CCH can activate the inflammasome signaling pathways, involving NLRP3 and AIM2 inflammasomes that critically regulate IL-1β production. Given that neuroinflammation is an early event in VCI, it is important that we understand its molecular and cellular mechanisms to enable development of disease-modifying treatments to reduce the structural brain damage and cognitive deficits that are observed clinically in the elderly. Hence, this review aims to provide a comprehensive insight into the molecular and cellular mechanisms involved in the pathogenesis of CCH-induced inflammasome signaling in VCI.
Source Title: MOLECULAR NEURODEGENERATION
URI: https://scholarbank.nus.edu.sg/handle/10635/218716
ISSN: 1750-1326
DOI: 10.1186/s13024-021-00506-8
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