期刊
ACS CHEMICAL NEUROSCIENCE
卷 13, 期 7, 页码 1002-1013出版社
AMER CHEMICAL SOC
DOI: 10.1021/acschemneuro.2c00005
关键词
Alzheimer's disease; amyloid-beta; olive leaf extract; oleuropein; neuroinflammation; NLRP3 inflammasome; RAGE; HGMB1; NF-kappa B pathway
资金
- Boundary Bend Olives Pty, Australia
Alzheimer's disease is the most common form of dementia among the elderly, characterized by Aβ plaque deposition, disrupted blood-brain barrier, and neuroinflammation. Olive leaf extract has been found to improve memory function by inhibiting inflammation, enhancing Aβ clearance, and improving blood-brain barrier integrity. Therefore, olive leaf extract may serve as a dietary supplement to prevent and slow down the progression of Alzheimer's disease.
Alzheimer's disease (AD) is the most common form of dementia among several neurodegenerative disorders afflicting the elderly. AD is characterized by the deposition of extracellular amyloid-beta (A beta) plaques, disrupted blood-brain barrier (BBB), and neuroinflammation. Several studies have demonstrated the health benefits of olive oil and olive leaf extract (OLE) due to their polyphenolic content. The main phenolic compound in OLE is glycosylated oleuropein (OLG), while the aglycon form of oleuropein (OLA) exists in much lower amounts. This work aimed to evaluate the effect of a low dose of OLG-rich OLE and the mechanism(s) that contributed to the observed beneficial effects against A beta pathology in the homozygous 5xFAD mouse model. Mice were fed with OLE-enriched diet (695 mu g/kg body weight/day) for 3 months, starting at 3 months old. Overall findings demonstrated that OLE reduced neuroinflammation by inhibiting the NF-kappa B pathway and suppressing the activation of NLRP3 inflammasomes and RAGE/HMGB1 pathways. In addition, OLE reduced total A beta brain levels due to increased clearance and reduced production of A beta and enhanced BBB integrity and function, which collectively improved the memory function. Thus, the consumption of OLE as a dietary supplement is expected to stop and/or slow the progression of AD.
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