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This research seeks to ascertain the kinetic parameters of VCO degradation based on the formation of peroxide and free fatty acids and to evaluate the shelf life of bromelain-extracted VCO at various temperatures. The kinetic parameters and shelf life of VCO were determined by measuring the value of peroxides and free fatty acids (FFA) concentration at temperatures of 50 ºC to 200 ºC. The heating was performed in a 1 L conical flask immersed in the paraffin bath. Samples were collected for each temperature at 0 to 60 minutes. The rate constant of peroxide and FFA formation was determined by regression analysis using Microsoft Excel, based on the plot of sampling time and value of peroxide and FFA concentration. The rate constant of peroxide formation escalated from 0.0114 to 0.1419 mEq Kg-1 min-1 when the VCO was heated at 50 ºC to 200 ºC. Meanwhile, the rate constant of FFA formation rose from 0.0188 to 0.0393 % min-1 when subjected to heating at 50 ºC to 200 ºC. Based on the shelf-life prediction established by Indonesian National Standards or the Asian and Pacific Coconut Community, the shelf-life of bromelain- extracted VCO varies from 10 to 3 hours at temperatures ranging from 2 ºC to 50 ºC. It was determined that elevating the temperature reduced the shelf-life of bromelain-extracted VCO. These findings suggest that temperature is crucial for the stability of bromelain-extracted VCO.

Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by cognitive impairment and neuronal death. The pathophysiology of AD includes cholinergic nerve damage, neuroinflammation, oxidative stress, and misfolding of amyloid-beta protein (Aβ). Current AD drug development focuses on a single target, whereas the AD mechanism is multifactorial, originating from the Aβ cascade, so intervention in Aβ is necessary. Flavonoid compounds are known to have many neuroprotective activities. Quercetin, an easily found flavonoid, can be used against AD. This research aimed to evaluate quercetin’s neuroprotective effect in inhibiting AD progression. In the in-vitro test, quercetin was assessed for its impact on inhibiting monomeric Aβ1-42 aggregation and inducing the disintegration of Aβ1-42 fibrils. Quercetin was also evaluated for its toxicity on differentiated human cholinergic cells (SH-SY5Y). Next, the neuroprotective effect of quercetin was tested in the same cells as Aβ1-42 induction. In-silico methods (Molecular docking and Molecular dynamics) were carried out to explain the molecular mechanism of drug action. In addition, druglikeness and ADMET parameters of flavonoids were predicted using SwissADME and pKCSM software. Quercetin is known to have a dual effect as an inhibitor of monomeric Aβ1-42 aggregation and a disintegrator of Aβ1-42 fibrils at concentrations of 10 µM – 200 µM. In molecular docking analysis, it is known that quercetin can bind to the hydrophobic part of Aβ1-42. Tests using molecular dynamics increasingly confirm that quercetin can disrupt the stability of Aβ1-42. In cell culture tests, quercetin was found to have a neuroprotective effect at an effective dose of 1-10 µM. ADMET parameters can also predict Quercetin and fulfill the Lipinski-Veber rule for predicting drug-likeness parameters. Quercetin has the potential to be developed as an anti-Alzheimer’s drug candidate with multi-target activity in the Aβ cascade.