Lauric Acid Alleviates Neuroinflammatory Responses by Activated Microglia: Involvement of the GPR40-Dependent Pathway

Your doctor needs to follow this closely to setup protocols to prevent your likely descent into dementia. Her responsibility, don't let her weasel her way out of it. I use coconut oil to fry my breakfast eggs and bake salmon in it. I use coconut milk as coffee creamer and the liquid for my oatmeal. Don't follow me, I'm not medically trained.

Your chances of getting dementia.

1. A documented 33% dementia chance post-stroke from an Australian study?

   May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.
3. A 20% chance in this research.   July 2013.

Lauric Acid Alleviates Neuroinflammatory Responses by Activated Microglia: Involvement of the GPR40-Dependent Pathway 

• Authors
• Authors and affiliations

• Yasunori Nishimura
• Mitsuaki MoriyamaEmail author
• Kenji Kawabe
• Hideyo Satoh
• Katsura Takano
• Yasu-Taka Azuma
• Yoichi Nakamura

• Yasunori Nishimura
  • 1
• Mitsuaki Moriyama
  • 1
  Email authorView author's OrcID profile
• Kenji Kawabe
  • 1
  • 2
• Hideyo Satoh
  • 1
• Katsura Takano
  • 1
• Yasu-Taka Azuma
  • 3
• Yoichi Nakamura
  • 1

1. 1.Laboratory of Integrative Physiology in Veterinary SciencesOsaka Prefecture UniversityIzumisanoJapan
2. 2.Department of Regenerative ScienceOkayama University Graduate School of Medicine, Dentistry and Pharmaceutical SciencesOkayamaJapan
3. 3.Laboratory of Veterinary PharmacologyOsaka Prefecture UniversityIzumisanoJapan

Original Paper

First Online: 26 June 2018

• 25 Downloads

Abstract

In several neurodegenerative diseases such as Alzheimer’s disease (AD), microglia are hyperactivated and release nitric oxide (NO) and proinflammatory cytokines, resulting its neuropathology. Mounting evidence indicates that dietary supplementation with coconut oil (CNO) reduces the cognitive deficits associated with AD; however, the precise mechanism(s) underlying the beneficial effect of CNO are unknown. In the present study, we examined the effects of lauric acid (LA), a major constituent of CNO, on microglia activated experimentally by lipopolysaccharide (LPS), using primary cultured rat microglia and the mouse microglial cell line, BV-2. LA attenuated LPS-stimulated NO production and the expression of inducible NO synthase protein without affecting cell viability. In addition, LA suppressed LPS-induced reactive oxygen species and proinflammatory cytokine production, as well as phosphorylation of p38-mitogen activated protein kinase and c-Jun N-terminal kinase. LA-induced suppression of NO production was partially but significantly reversed in the presence of GW1100, an antagonist of G protein-coupled receptor (GPR) 40, which is an LA receptor on the plasma membrane. LA also decreased LPS-induced phagocytosis, which was completely reversed by co-treatment with GW1100. Moreover, LA alleviated amyloid-β-induced enhancement of phagocytosis. These results suggest that attenuation of microglial activation by LA may occur via the GPR40-dependent pathway. Such effects of LA may reduce glial activation and the subsequent neuronal damage in AD patients who consume CNO.