Neuroinflammation, Resolution, and Neuroprotection in the Brain

Table of Contents

1. Molecular aspects of neuroinflammation: Contribution of eicosanoids, cytokines and chemokines 2. Contribution of bioactive lipids mediators in neuroinflammation, resolution, and neuroprotection 3. Contribution of protein-derived bioactive molecules (cytokines and chemokines) in neuroinflammation, resolution, and neuroprotection 4. Contribution of neuroinflammation, resolution, and neuroprotection in neurotraumatic diseases 5. Contribution of neuroinflammation, resolution, and neuroprotection in neurodegenerative diseases 6. Contribution of neuroinflammation, resolution, and in neuropsychiatric diseases 7. Regulation of neuroinflammation, resolution, and neuroprotection by diet and gut microbiota 8. Regulation of neuroinflammation, resolution, and neuroprotection by aerobic exercise, yoga, and tai-chi 9. Prevention of neuroinflammation and resolution by phytochemicals 10. Effects of dietary patterns, exercise on neuroinflammation: Perspective and future studies

Authors

Akhlaq A. Farooqui Research Scientist, Department of Molecular and Cellular Biochemistry, The Ohio State University, Columbus, OH, USA. Akhlaq A. Farooqui is a leader in the field of signal transduction processes, lipid mediators, phospholipases, glutamate neurotoxicity, and neurological disorders. He is a research scientist in the Department of Molecular and Cellular Biochemistry at The Ohio State University. He has published cutting edge research on the role of phospholipases A2 in signal transduction processes, generation and identification of lipid mediators during neurodegeneration by lipidomics. He has studied the involvement of glycerophospholipid, sphingolipid-, and cholesterol-derived lipid mediators in kainic acid neurotoxicity, an experimental model of neurodegenerative diseases. Akhlaq A. Farooqui has discovered the stimulation of plasmalogen- selective phospholipase A2 in brains of patients with Alzheimer disease (AD). Stimulation of this enzyme may not only be responsible for the deficiency of plasmalogens in neural membranes of AD patients, but also be related to the loss of synapse in the AD.