Amyloid cascade hypothesis is the main theoretical framework describing the development of Alzheimer's disease (AD). However, most clinical trials of therapy targeting amyloid-β peptide (Aβ) are unsuccessful because AD is a complex disease involving many genetic and environmental factors. Among various factors, inflammation within the brain in particular has been implicated in the pathogenesis and progression of AD. Furthermore, it has been shown that systemic inflammation can initiate AD. Therefore, anti-inflammatory agents might be beneficial for prevention and/or treatment of AD. Many reports have indicated that luteolin, a flavone found in various foods, has preventive and therapeutic value for neurodegenerative diseases including AD. Such effect of luteolin has been linked to its ability to relieve neuroinflammation. Luteolin also has other biological functions, including antioxidant activity that may provide added benefit for prevention of AD. The exact mechanisms of inflammatory pathways involved in AD pathogenesis need to be further understood to utilize luteolin and many other available anti-inflammatory agents to prevent and treat AD. In addition, it is critical to develop better experimental models that resemble the inflammatory conditions in clinical AD.
Keywords: Alzheimer's disease; Anti-inflammatory agents; Inflammation; Luteolin.
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