Evaluation of possible neuroprotective effects of virgin coconut oil on aluminum‐induced neurotoxicity in an in vitro Alzheimer's disease model

• Published in: Journal of applied toxicology 2024-04, Vol.44 (4), p.609-622
• Main Authors: Demirel, Göksun, Sanajou, Sonia, Yirün, Anil, Çakir, Deniz Arca, Berkkan, Aysel, Baydar, Terken, Erkekoğlu, Pinar
• Format: Article
• Language: English
• Subjects: Acetylcholinesterase; Acetylcholinesterase - metabolism; Aluminum; Aluminum - toxicity; Alzheimer Disease - chemically induced; Alzheimer Disease - drug therapy; Alzheimer's disease; Amyloid beta-Peptides - toxicity; Amyloid precursor protein; Brain-derived neurotrophic factor; Carbonyl compounds; Carbonyls; Coconut oil; Coconut Oil - pharmacology; Cognitive ability; Dopamine; Dopamine transporter; Environmental factors; Exposure; Humans; Lipids; Mathematical models; Neuroblastoma; Neurodegenerative diseases; Neurological diseases; Neuroprotection; Neuroprotective agents; Neuroprotective Agents - pharmacology; Neuroprotective Agents - therapeutic use; Neurotoxicity; neurotransmitter; Neurotransmitter Agents; Neurotransmitters; Oxidative stress; Parameters; Peroxidase; Proteins; Reactive oxygen species; Retinoic acid; Synuclein; Tau protein; β-Amyloid
• ISSN: 0260-437X; 1099-1263
• DOI: 10.1002/jat.4564

Alzheimer's disease (AD) is a progressive neurological disorder that affects various cognitive functions, behavior, and personality. AD is thought to be caused by a combination of genetic and environmental factors, including exposure to aluminum (Al). Virgin coconut oil (VCO) may have potential as a natural neuroprotectant against AD. Aim of this study was to determine neuroprotective effects of VCO on Al‐induced neurotoxicity in an in vitro AD model. SH‐SY5Y cells were initially cultured in normal growth medium and then differentiated by reducing fetal bovine serum content and adding retinoic acid (RA). Later, brain‐derived neurotrophic factor (BDNF) was added along with RA. The differentiation process was completed on the seventh day. Study groups (n = 3) were designed as control group, VCO group, Al group, Al‐VCO group, Alzheimer model (AD) group, AD + Al‐exposed group (AD+Al), AD + VCO applied group (AD + VCO) and AD + Al‐exposed + VCO applied group (AD + Al + VCO). Specific markers of AD (hyperphosphorylated Tau protein, amyloid beta 1–40 peptide, and amyloid precursor protein) were measured in all groups. In addition, oxidative stress parameters (total antioxidant capacity, lipid peroxidase, protein carbonyl, and reactive oxygen species) and neurotransmitter‐related parameters (dopamine, dopamine transporter acetylcholine, and synuclein alpha levels, acetylcholinesterase activity) were measured comparatively in the study groups. VCO reduced amyloid beta and hyperphosphorylated Tau protein levels in the study groups. In addition, oxidative stress levels decreased, and neurotransmitter parameters improved with VCO. Our study shows that VCO may have potential therapeutic effects in Alzheimer's disease and further experiments are needed to determine its efficacy. The aim of this study was to investigate the neuroprotective effects of virgin coconut oil (VCO) on aluminum‐induced neurotoxicity in an in vitro model of Alzheimer's disease (AD). Specific markers of AD, oxidative stress parameters, and neurotransmitter‐related parameters were measured. VCO reduced amyloid beta and hyperphosphorylated Tau protein levels, reduced oxidative stress, and improved neurotransmitter parameters. These findings suggest that VCO may have potential therapeutic effects in Alzheimer's disease, but further experiments are needed to determine its efficacy.