Insulin Resistance as a Risk Factor in Visceral and Neurological Disorders provides an overview on the risk factors for insulin resistance in visceral and neurological disorders. The book focuses on molecular mechanisms and signal transduction processes associated with the links. The comprehensive information in this monograph will not only help in the early detection of insulin resistance related visceral and neurological disorders, but also promote the discovery of new drugs which may block or delay onset in elderly patients. Understanding these processes is important not only for patients, caregivers and health professionals, but also for health policymakers who must plan for national resources.
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2. Insulin resistance, diabetes, and metabolic syndrome
3. Insulin resistance and heart disease
4. Insulin resistance and sleep apnea
5. Insulin resistance and stroke
6. Insulin resistance and Alzheimer's disease
7. Insulin resistance and Parkinson's disease
8. Insulin resistance, dementia, and depression
9. Use of phytochemicals for the treatment of insulin resistance-linked visceral and neurological disorders
10. Summary and perspective for future research on insulin resistance and insulin resistance-linked visceral and neurological disorders
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.