Olive Oil Polyphenol Oleuropein Shows Promising Neuroprotective Effects in Cellular Model of Parkinson’s Disease

Recent study findings suggested that oleuropein possesses neuroprotective effects in an in vitro model of PD when administered preventively as a pre-treatment.

By Negar Jamshidi
Sep. 6, 2016 13:51 UTC

Described as the sec­ond most com­mon neu­rode­gen­er­a­tive dis­or­der, Parkinson’s dis­ease (PD) has long been asso­ci­ated with high lev­els of oxida­tive stress. The pri­mary char­ac­ter­is­tic of PD is a pro­gres­sive loss of neu­ro­trans­mit­ter dopamine and neu­ronal degen­er­a­tion lead­ing to the devel­op­ment of motor symp­toms.

Oxidative stress results from an accu­mu­la­tion of reac­tive oxy­gen species (ROS) and evi­dence sug­gests that it con­tributes to the patho­gen­e­sis of PD by affect­ing the mito­chon­dr­ial dys­func­tion, apop­to­sis, inflam­ma­tory response or lyso­so­mal degra­da­tion (autophagy) path­ways.
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In par­tic­u­lar, since the autophagy-lyso­so­mal path­way is known to be the cen­tral cel­lu­lar mech­a­nism for pro­tein aggre­gate degra­da­tion and removal of dam­aged mito­chon­dria, dis­rup­tion of the autophagy-lyso­so­mal path­way by ROS has been impli­cated in the patho­gen­e­sis of PD and of great inter­est as a ther­a­peu­tic tar­get.

The main chal­lenge with the treat­ment of PD is due to the late clin­i­cal pre­sen­ta­tion when neu­ronal loss has already occurred, thus efforts are con­cen­trated on find­ing strate­gies that pro­tect or halt neu­ron loss.

Increasing evi­dence has shown nat­ural polyphe­nols such as cat­e­chins, resver­a­trol and isoflavons exert neu­ro­pro­tec­tive effects by decreas­ing oxida­tive stress, inflam­ma­tion and neu­ron death (apop­to­sis). In par­tic­u­lar, oleu­ropein (OLE), one of the major phe­no­lic com­po­nents of olive oil, has been demon­strated to have a broad spec­trum of ther­a­peu­tic ben­e­fits includ­ing anti-inflam­ma­tory, anti-oxi­dant, anti-can­cer as well as antimi­cro­bial activ­i­ties.

Of inter­est, OLE has been found to reduce apop­to­sis and ROS gen­er­a­tion in pre­clin­i­cal mod­els. Recent find­ings of a study pub­lished in the International Journal of Molecular Science indi­cated treat­ment of neu­ronal PC12 cells with OLE not only low­ered oxida­tive stress lev­els and apop­to­sis but also mod­u­lated the autophagy process.

The researchers ini­tially treated cells with OLE before the addi­tion of a potent Parkinson toxin (6‑OHDA) demon­strat­ing sig­nif­i­cant reduc­tion in neu­ron cell death, and con­cluded that these results endorse OLE as a pro-sur­vival mol­e­cule play­ing a pre­ven­tive pro-sur­vival role in our cel­lu­lar par­a­digm.”

Further data in sup­port of the neu­ro­pro­tec­tive effect of OLE was obtained when the same cel­lu­lar model was treated with OLE before the addi­tion of a pow­er­ful inhibitor of the super­ox­ide dis­mu­tase enzyme (known as DDC), result­ing in a con­sid­er­able reduc­tion in mito­chon­dr­ial super­ox­ide pro­duc­tion.

Next, the researchers assessed bio­marker expres­sion spe­cific to the autophagy process. Their data sug­gested OLE plays a novel role in pre­vent­ing autophagy stim­u­la­tion by affect­ing the expres­sion lev­els of pro­teins involved in the lyso­so­mal path­way.

The authors cau­tioned that while these results sup­port a role for OLE as a mod­u­la­tor of the autophagic flux, autophagy acti­va­tion is also linked to neu­ronal death” and there­fore the exact role and use of OLE in lyso­so­mal degra­da­tion path­way requires fur­ther research before clin­i­cal trans­la­tion as a ther­a­peu­tic tar­get of the autophagy process.

The final take-home mes­sage of the study was that these data solid­ify oleu­ropein as a can­di­date for the devel­op­ment of novel pre­ven­tive ther­a­pies in neu­rode­gen­er­a­tive dis­eases with a facet of oxida­tive stress and/or impair­ment of autophagy, such as in Parkinson’s Disease.”


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