Alzheimer’s disease (AD) is a debilitating neurodegenerative disease characterized by cognitive decline and currently affects more than 50 million people worldwide and puts a massive strain on the health care system of a country.¹ The incident rate of AD increases substantially with age, with only 2% at 65 years of age, 13% at 90 years of age, and 21% at 95 years of age, respectively.² As a result, developed countries with large ageing populations are predicted to take the most strain.

AD is a multi-factorial disease believed to be caused by a combination of genetic, environmental and lifestyle factors. The hallmarks of AD refer to the deposition of amyloid-β (Aβ), or plaques, outside neurons which disrupt communication between brain cells, and trigger inflammation and twisted strands of the protein ‘tau’ inside neurons, which contribute to neurodegeneration in the brain.³

There is currently no cure for AD, only a range of medications that may slow the progression of the disease or improve symptoms. Unfortunately, available drugs are not very effective and have adverse side effects.¹ As a result, there is a large drive to study AD, its risk factors, preventative measures as well as possible treatments. In this article, we look at how coffee and extra virgin olive oil can play a role in the prevention of AD.

The pro-inflammatory and amyloidogenic (growth of amyloid structures) protein S100A9 is a significant contributor to both the amyloid and neuroinflammatory pathways in AD. During inflammation, the level of S100A rises and may affect its amyloid self-assembly and tissue damage, which is seen in neurodegenerative diseases. In AD, S100A9 assembles with Aβ, leading to the build-up of amyloid inside of the cells and amyloid plaque growth outside of the neural cells. Since the whole amyloid pathway can potentially be altered or reversed by targeting the S100A9 protein, it is a possible target for treatments for AD.⁵

Special attention has been placed on oleuropein and its derivatives which are present in high quantities in EVOO as they offer protective functionalities, including anti-oxidant, anti-viral, anti-tumour, antimicrobial, cardio-protective, neuroprotective, anti-ageing, anti-diabetic, and anti-inflammatory effects. Polyphenol oleuropein aglycone (OleA) is the most abundant compound in EVOO and can inhibit S100A9 amyloid accumulation in several ways as well as break apart already-formed fibrils, converting them into non-toxic aggregates. Through these mechanisms, OleA alleviates the consequences of the amyloid-neuroinflammatory pathway caused by the S100A9 in neurodegenerative diseases.⁵

The expression of BMI1 (B lymphoma Mo-MLV insertion region 1 homolog) has a significant neuroprotective effect as it causes the activation of antioxidant defenses and suppression of Reactive Oxidative Species (ROS) levels. The big question is whether BMI1 has a significant role in AD and if EVOO could be used to reverse the onset of AD. EVOO treatment in patients with Mild Cognitive Impairment for 12 months increased BMI1 levels, lowered p53 levels, and the levels of AD biomarkers (markers indicating the presence of AD) returned to normal. The onset of neurodegenerative diseases is driven by neuroinflammation; two common hallmarks of neuroinflammation include Tumor Necrosis Factor Alpha (TNF-α) and Interleukin-6 (IL-6). Not surprisingly, IL-6 levels are increased in AD due to the presence of Aβ plaques. EVOO treatment for a year was shown to prevent the increase of IL-6 and TNF-α levels (reducing the inflammatory and oxidative stress responses), which also correlates with BMI1 restoration. As you can see EVOO contains many beneficial compounds and may have the potential to work as an alternative therapy for preventing the onset of AD.⁶