@article {46916,
	title = {Role of dietary fatty acids in microglial polarization in Alzheimer{\textquoteright}s disease},
	volume = {17},
	year = {2020},
	month = {MAR},
	pages = {93},
	type = {Review},
	abstract = {<p>Microglial polarization is an utmost important phenomenon in Alzheimer{\textquoteright}s disease that influences the brain environment. Polarization depends upon the types of responses that cells undergo, and it is characterized by receptors present on the cell surface and the secreted cytokines to the most. The expression of receptors on the surface is majorly influenced by internal and external factors such as dietary lipids. Types of fatty acids consumed through diet influence the brain environment and glial cell phenotype and types of receptors on microglia. Reports suggest that dietary habits influence microglial polarization and the switching of microglial phenotype is very important in neurodegenerative diseases. Omega-3 fatty acids have more influence on the brain, and they are found to regulate the inflammatory stage of microglia by fine-tuning the number of receptors expressed on microglia cells. In Alzheimer{\textquoteright}s disease, one of the pathological proteins involved is Tau protein, and microtubule-associated protein upon abnormal phosphorylation detaches from the microtubule and forms insoluble aggregates. Aggregated proteins have a tendency to propagate within the neurons and also become one of the causes of neuroinflammation. We hypothesize that tuning microglia towards anti-inflammatory phenotype would reduce the propagation of Tau in Alzheimer{\textquoteright}s disease.</p>
},
	keywords = {Fatty acids, Microglial polarization, Omega-3 fatty acids, Tau inflammation, Tau phagocytosis, Tau spreading, Tauopathy},
	doi = {10.1186/s12974-020-01742-3},
	author = {Desale, Smita Eknath and Chinnathambi, Subashchandrabose}
}
@article {47124,
	title = {Alpha-Linolenic acid modulates phagocytosis and endosomal pathways of extracellular Tau in microglia},
	journal = {Cell Adhesion \& Migration},
	volume = {15},
	year = {2021},
	month = {JAN },
	pages = {84-100},
	type = {Article},
	abstract = {<p>Microglia, the resident immune cells, were found to be activated to inflammatory phenotype in Alzheimer{\textquoteright}s disease (AD). The extracellular burden of amyloid-beta plaques and Tau seed fabricate the activation of microglia. The seeding effect of extracellular Tau species is an emerging aspect to study about Tauopathies in AD. Tau seeds enhance the propagation of disease along with its contribution to microglia-mediated inflammation. The excessive neuroinflammation cumulatively hampers phagocytic function of microglia reducing the clearance of extracellular protein aggregates. Omega-3 fatty acids, especially docosahexaenoic acid and eicosapentaenoic acid, are recognized to induce anti-inflammatory phenotype of microglia. In addition to increased cytokine production, omega-3 fatty acids enhance phagocytic receptors expression in microglia. In this study, we have observed the phagocytosis of extracellular Tau in the presence of alpha-linolenic acid (ALA). The increased phagocytosis of extracellular Tau monomer and aggregates have been observed upon ALA exposure to microglia cells. After internalization, the degradation status of Tau has been studied with early and late endosomal markers Rab5 and Rab7. Further, the lysosome-mediated degradation of internalized Tau was studied with LAMP-2A, a lysosome marker. The enhanced migratory ability in the presence of ALA could be beneficial for microglia to access the target and clear it. The increased migration of microglia was found to induce the microtubule-organizing center repolarization. The data indicate that the dietary fatty acids ALA could significantly enhance phagocytosis and intracellular degradation of internalized Tau. Our results suggest that microglia could be influenced to reduce extracellular Tau seed with dietary fatty acids.</p>
},
	keywords = {alpha-linolenic acid, endosomal markers, Fatty acids, MTOC repolarization, Phagocytosis, Tauopathy},
	issn = {1933-6918},
	doi = {10.1080/19336918.2021.1898727},
	author = {Desale, Smita Eknath and Chinnathambi, Subashchandrabose}
}
