Schisantherin A is a dibenzocyclooctadiene originally found in Schisandra that exhibits anti-tussive, sedative, anti-inflammatory, anti-osteoporotic, neuroprotective, cognition enhancing, and cardioprotective activities. In macrophages, schisantherin A decreases LPS-induced expression and activity of iNOS, COX-2, NO, IL-6, and TNF-α. Schisantherin A also decreases RANKL-induced NF-κB signaling by inhibiting IκBα degradation and suppressing JNK and ERK1/2 activation in vitro; it also inhibits osteoclast function and bone erosion in vivo. In animal models of Alzheimer’s disease, schisantherin A inhibits amyloid-β (Aβ)-induced learning and memory impairments in Y maze, shuttle box, and Morris water maze assays. Additionally, this compound lowers left ventricular systolic and end diastolic pressures, decreases infarct size and maldionaldehyde release, and increases superoxide dismutase activity, preventing myocardial apoptosis in animal models of cardiac ischemia/reperfusion. Schisantherin A conferred significant protection against MPTP-induced loss of TH-positive dopaminergic neurons in a Parkinson's disease (PD) mice model. Western blotting analysis demonstrated that Schisantherin A exhibited neuroprotection against MPP(+) through the regulation of two distinct pathways including increasing CREB-mediated Bcl-2 expression and activating PI3K/Akt survival signaling suggesting that StA might be a promising neuroprotective agent for the prevention of PD.