Abstract
Alzheimer’s disease (AD) is a neurodegenerative disorder that is characterised by the presence of extracellular beta-amyloid fibrillary plaques and intraneuronal neurofibrillary tau tangles in the brain. Recurring failures of drug candidates targeting these pathways have prompted research in AD multifactorial pathogenesis, including the role of neuroinflammation. Triggered by various factors, such as hypoxia, neuroinflammation is strongly linked to AD susceptibility and/or progression to dementia. Chronic hypoxia induces neuroinflammation by activating microglia, the resident immune cells in the brain, along with an increased in reactive oxygen species and pro-inflammatory cytokines, features that are common to many degenerative central nervous system (CNS) disorders. Hence, interests are emerging on therapeutic agents and plant derivatives for AD that target the hypoxia-neuroinflammation pathway. Centella asiatica is one of the natural products reported to show neuroprotective effects in various models of CNS diseases. Here, we review the complex hypoxia-induced neuroinflammation in the pathogenesis of AD and the potential application of Centella asiatica as a therapeutic agent in AD or dementia.
Highlights
Millions around the world are suffering from various forms of neurodegenerative diseases
Previous studies reported that neuroinflammation is one of Alzheimer’s disease (AD) hallmark pathophysiological features and is increasingly recognised as a potential therapeutic target of this neurodegenerative disease, recently
It has been shown that neuroinflammation can be acquired in the hypoxic condition via several pathways, including NF-κβ and Nuclear factor erythroid 2-like factor 2 (Nrf2)
Summary
Millions around the world are suffering from various forms of neurodegenerative diseases AD may result from a combination of aetiologies, but the most widely accepted pathological hallmarks are deposition of amyloid plaques and neurofibrillary tangles (Hardy and Allsop, 1991; Goedert, 1993; Lane et al, 2018) Other than these two, neuroinflammation has been implicated in the pathogenesis of AD (Morales et al, 2014). The expression of multiple receptors of pro-inflammatory mediators, including cytokines, chemokines and damage signals, on astrocytes was upregulated within this inflammatory response (Krasowska-Zoladek et al, 2007), indicating that a secondary inflammatory response occurs as astrocytes are being activated in response to those pro-inflammatory mediators (Morales et al, 2014) Both Aβ deposition and neuroinflammation can be the initiator to one and another causes these detrimental conditions may worsen in the long run, which contribute to a cascade of other pathological hallmarks of AD, and eventually develop AD
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