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The activation of Nrf2 by lutein may be caused by the presence of an electrophilic group that combines with the cysteine residue thiols in Keap1 to cause the Nrf2-Keap1 complex to break down, thereby boosting the production of different cytoprotective and antioxidant proteins and supporting their cardioprotective properties

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Notably, in addition to its anti-AChE activity, ()-Phen is able to inhibit the synthesis of amyloid precursor protein (APP) and alpha-synuclein (-syn), proteins of consequence in the pathology of AD and PD, respectively, and of currently increasing relevance to TBI in light of the up regulation of pathways leading to AD and PD in animal models of TBI [9,10,11,12] and in light of increased risk for early onset dementia and PD in humans suffering TBI [7, 8, 65,66,67]