Abstract
Alzheimer’s disease (AD) is a common neurodegenerative disease and a major contributor to progressive cognitive impairment in an aging society. As the pathophysiology of AD involves chronic neuroinflammation, the resolution of inflammation and the group of lipid mediators that actively regulate it—i.e., specialized pro-resolving lipid mediators (SPMs)—attracted attention in recent years as therapeutic targets. This review focuses on the following three specific SPMs and summarizes their relationships to AD, as they were shown to effectively address and reduce the risk of AD-related neuroinflammation: maresin 1 (MaR1), resolvin D1 (RvD1), and neuroprotectin D1 (NPD1). These three SPMs are metabolites of docosahexaenoic acid (DHA), which is contained in fish oils and is thus easily available to the public. They are expected to become incorporated into promising avenues for preventing and treating AD in the future.
Highlights
Alzheimer’s disease (AD) is currently the most common cause of dementia [1]
In addition to an overview of specialized pro-resolving lipid mediators (SPMs) in general, we focus on three produced in the human brain: maresin 1 (MaR1), resolvin D1 (RvD1), and neuroprotectin D1 (NPD1) [50,55,56]
MaR1 up-regulates the level of microglia that are down-regulated by Aβ in the course of AD [122]; in the context of the RvD1- and lipoxin A4 (LXA4)-mediated increase in the microglial phagocytosis of Aβ by the action of, this finding suggests that MaR1 plays a distinct role in the microglia-mediated removal of Aβ [50]. These findings suggest that the induction of MaR1 could be a novel, effective approach to treat AD
Summary
Alzheimer’s disease (AD) is currently the most common cause of dementia [1]. While cholinesterase inhibitors and N-methyl-D-aspartate (NMDA) receptor antagonists are typically used to attenuate the symptoms and progression of dementia, they do not provide complete treatment nor do any other therapies, till date. Characterized by the deposition of amyloid-β (Aβ) outside neurons [3,4,5,6,7,8] and hyperphosphorylated tau proteins within [9], the pathology of AD is largely ascribed to the activation of immune system, such as microglia [10,11,12], which leads to neuroinflammation induced by the disruption of hypothalamic-pituitary-adrenal hormonal homeostasis by various chronic stress factors [13], including infection, invasive injury, and autoimmune response [14,15,16,17,18,19,20]. Aβ activates microglia and astrocytes, causing chronic inflammation [15]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
