Seminar: Linoleic acid participates in the response to ischemic brain injury through oxidized metabolites that regulate neurotransmission

SIMR-Meeting Room (M-32) 28 MAR 20171 PM

Linoleic acid participates in the response to ischemic brain injury through oxidized metabolites that regulate neurotransmission

Ameer Y. Taha

Department of Food Science and Technology, University of California Davis, CA, USA

Omega-6 linoleic acid (LA) has become ubiquitous in our diets due to agricultural shifts towards high LA soybean and corn oils, resulting in a 3- to 5- fold increase in LA intake over the past few decades. Despite being a dietary stipulate, LA has been considered a benign fatty acid in the brain because of its low concentration (<2%) relative to other polyunsaturated fatty acids such as arachidonic and docosahexaenoic acid. LA, however, crosses the blood brain barrier at a rate comparable to other polyunsaturated fatty acids. It is also a precursor to oxygenase-derived oxidized linoleic acid metabolites (OXLAMs) known to regulate calcium signaling in peripheral tissue. The role(s) of LA or OXLAMs in brain are not known. The present series of rodent studies tested the hypothesis that LA entering the brain is converted into OXLAMs that regulate signaling. Increasing dietary LA increased brain OXLAM concentrations and minimally altered brain LA levels, suggesting preferential conversion of LA into OXLAMs rather than incorporation upon entering the brain. Brain injury caused by ischemia increased the formation of OXLAMs such as 13-hydroxyoctadecadienoic acid, which was subsequently found to increase somatic paired pulse facilitation in hippocampal slices. These findings provide new evidence that dietary LA is a key regulator of brain bioactive lipid mediators (OXLAMs) which participate in the response to brain injury and neurotransmission. Targeting this signaling pathway with dietary LA lowering or drugs may yield novel treatments for ischemic stroke and other neurodegenerative disorders.


Dr. Taha, an assistant professor in the Department of Food Science and Technology at UC Davis, specializes in food chemistry and neurochemistry. Dr. Taha completed his Ph.D. in Pharmacology and Toxicology at the University of Toronto in Canada. He joined UC Davis in 2014 after completing a postdoctoral fellowship at National Institutes of Health in Bethesda, Maryland, USA. Dr. Taha's research is focused on understanding the role of oxidized fatty acids on brain signaling and neurodegenerative disorders. His work has unveiled a new brain lipid signaling pathway that might contribute to inflammation present in many neurodegenerative disorders. Dr. Taha's lab is currently testing novel drugs that target this new pathway to treat neuroinflammation.

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