Molecular Aspects of Neurodegeneration, Neuroprotection, and Regeneration in Neurological Disorders

Table of Contents

1. Molecular aspects of neurodegeneration and classification of neurological disorders2. Effect of diet on neurological disorders and regenerative processes in the brain3. Molecular mechanisms of neurodegeneration in neurotraumatic diseases4. Molecular mechanisms of neurodegeneration in neurodegenerative diseases 5. Molecular mechanisms of neurodegeneration in neuropsychiatric diseases6. Molecular aspects of regeneration and neuroprotection in neurotraumatic diseases7. Molecular aspects of regeneration and neuroprotection in neurodegenerative diseases 8. Molecular aspects of regeneration and neuroprotection in neuropsychiatric diseases9. Strategies for the potential treatment of neurological disorders with Chinese and Indian medicinal plants10. Summary, perspective, and future studies on neurodegeneration and regeneration in neurological disorders

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.