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How fisetin reduces the impact of age and disease on CNS function
Pamela Maher1,*
1
The Salk Institute for Biological Studies, 10010 N. Torrey Pines Rd, La Jolla, CA 92037
DOI: 10.2741/S425 Volume 7 Issue 1, pp.58-82
Published: 01 June 2015
(This article belongs to the Special Issue Aging, neuroinflammation and neurodegeneration)
*Corresponding Author(s):  
Pamela Maher
E-mail:  
pmaher@salk.edu
Abstract

It is becoming increasingly clear that neurological diseases are multi-factorial involving disruptions in multiple cellular systems. Thus, while each disease has its own initiating mechanisms and pathologies, certain common pathways appear to be involved in most, if not all, neurological diseases. Thus, it is unlikely that modulating only a single factor will be effective at either preventing disease development or slowing disease progression. A better approach is to identify small (< 900 daltons) molecules that have multiple biological activities relevant to the maintenance of brain function. We have identified an orally active, novel neuroprotective and cognition-enhancing molecule, the flavonoid fisetin. Fisetin not only has direct antioxidant activity but it can also increase the intracellular levels of glutathione, the major intracellular antioxidant. Fisetin can also activate key neurotrophic factor signaling pathways. In addition, it has anti-inflammatory activity and inhibits the activity of lipoxygenases, thereby reducing the production of pro-inflammatory eicosanoids and their by-products. This wide range of actions suggests that fisetin has the ability to reduce the impact of age-related neurological diseases on brain function.

Key words
Oxidative Stress, Glutathione, Neurotrophic Factors, Memory, Microglia, Inflammation, Review
Share and Cite
Pamela Maher. How fisetin reduces the impact of age and disease on CNS function. Frontiers in Bioscience-Scholar. 2015. 7(1); 58-82.