Neuroinflammation, Resolution, and Neuroprotection in the Brain
Sep 2021 · Academic Press
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332
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Über dieses E-Book
Neuroinflammation, Resolution, and Neuroprotection in the Brain discusses the molecular aspects of neuroinflammation in neurological disorders. The book examines the effect of diet and exercise on neuroinflammatory diseases. Chapters focus on bioactive lipids, cytokines and chemokines, as well as the involvement of neuroinflammation, resolution and neuroprotection in neurotraumatic diseases, neurodegenerative diseases and neuropsychiatric diseases. The comprehensive information in this monograph will help readers understand molecular cross-talk among mediators of phospholipid, sphingolipid and cholesterol metabolism. The book's goal is to jumpstart more studies on molecular mechanisms and the therapeutic aspects of neurological disorders in human subjects. - Discusses the molecular aspects of neuroinflammation, resolution and neuroprotection - Examines the role of diet and exercise on neuroinflammatory diseases - Provides cutting-edge research on signal transduction processes - Explores the treatment of neurological disorders caused by neuroinflammation
Autoren-Profil
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.
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