Neurochemical Aspects of Neurotraumatic and Neurodegenerative Diseases (eBook)
XXIII, 401 Seiten
Springer New York (Verlag)
978-1-4419-6652-0 (ISBN)
Dr. Akhlaq A. Farooqui is a leader in the field of brain phospholipases A2, bioactive ether lipid metabolism, polyunsaturated fatty acid metabolism, glycerophospholipid-, sphingolipid-, and cholesterol-derived lipid mediators, glutamate-induced neurotoxicity and neurological disorders. He has discovered the stimulation of plasmalogen-selective phospholipase A2 (PlsEtn-PLA2) in brains from patients with Alzheimer disease. Stimulation of PlsEtn-PLA2 produces plasmalogen deficiency and increases levels of eicosanoids that may be related to the loss of synapses, induction of neuroinflammation and oxidative stress in brains of patients with Alzheimer disease. Dr. Farooqui has published cutting edge research on the generation and identification of glycerophospholipid-, sphingolipid-, and cholesterol-derived lipid mediators in kainic acid neurotoxicity by lipidomics. He has previously authored five monographs: Glycerophospholipids in Brain: Phospholipase A2 in Neurological Disorders (2007); Neurochemical Aspects of Excitotoxicity (2008); Metabolism and Functions of Bioactive Ether Lipids in Brain (2008); Hot Topics in Neural Membrane Lipidology (2009), and Beneficial Effects of Fish Oil on Human Brain (2009). All monographs are published by Springer. Dr. Farooqui has also edited two books: 'Biogenic Amines: Pharmacological, Neurochemical and Molecular Aspects in the CNS' Nova Science Publishers, Hauppauge, N.Y (2010) and Molecular Aspects of Neurodegeneration and Neuroprotection, Bentham Science Publishers Ltd (2010).
Collectively, neurodegenerative diseases are characterized by chronic and progressive loss of neurons in discrete areas of the brain, producing debilitating symptoms such as dementia, loss of memory, loss of sensory or motor capability, decreased overall quality of life eventually leading to premature death. Two types of cell death are known to occur during neurodegeneration: (a) apoptosis and (b) necrosis. The necrosis is characterized by the passive cell swelling, intense mitochondrial damage with rapid loss of ATP, alterations in neural membrane permeability, high calcium influx, and disruption of ion homeostasis. This type of cell death leads to membrane lysis and release of intracellular components that induce inflammatory reactions. Necrotic cell death normally occurs at the core of injury site. In contrast, apoptosis is an active process in which caspases (a group of endoproteases with specificity for aspartate residues in protein) are stimulated. Apoptotic cell death is accompanied by cell shrinkage, dynamic membrane blebbing, chromatin condensation, DNA laddering, loss of phospholipids asymmetry, low ATP levels, and mild calcium overload. This type of cell death normally occurs in penumbral region at the ischemic injury site and in different regions in various neurodegenerative diseases.
Dr. Akhlaq A. Farooqui is a leader in the field of brain phospholipases A2, bioactive ether lipid metabolism, polyunsaturated fatty acid metabolism, glycerophospholipid-, sphingolipid-, and cholesterol-derived lipid mediators, glutamate-induced neurotoxicity and neurological disorders. He has discovered the stimulation of plasmalogen-selective phospholipase A2 (PlsEtn-PLA2) in brains from patients with Alzheimer disease. Stimulation of PlsEtn-PLA2 produces plasmalogen deficiency and increases levels of eicosanoids that may be related to the loss of synapses, induction of neuroinflammation and oxidative stress in brains of patients with Alzheimer disease. Dr. Farooqui has published cutting edge research on the generation and identification of glycerophospholipid-, sphingolipid-, and cholesterol-derived lipid mediators in kainic acid neurotoxicity by lipidomics. He has previously authored five monographs: Glycerophospholipids in Brain: Phospholipase A2 in Neurological Disorders (2007); Neurochemical Aspects of Excitotoxicity (2008); Metabolism and Functions of Bioactive Ether Lipids in Brain (2008); Hot Topics in Neural Membrane Lipidology (2009), and Beneficial Effects of Fish Oil on Human Brain (2009). All monographs are published by Springer. Dr. Farooqui has also edited two books: “Biogenic Amines: Pharmacological, Neurochemical and Molecular Aspects in the CNS” Nova Science Publishers, Hauppauge, N.Y (2010) and Molecular Aspects of Neurodegeneration and Neuroprotection, Bentham Science Publishers Ltd (2010).
Preface 5
Acknowledgments 8
Contents 9
About the Author 16
List of Abbreviations 17
1 Neurodegeneration in Neural Trauma, Neurodegenerative Diseases, and Neuropsychiatric Disorders 18
1.1 Introduction 18
1.2 Neurodegeneration in Ischemic Injury 24
1.3 Neurodegeneration in Traumatic Brain Injury and Spinal Cord Trauma 26
1.4 Neurodegeneration in Neurodegenerative Diseases 26
1.5 Neurodegeneration in Neuropsychiatric Diseases 31
1.6 Similarities and Differences Between Ischemic, Neurotraumatic Injuries, Neurodegenerative Diseases, and Neuropsychiatric Disorders 32
1.7 Conclusion 37
References 38
2 Neurochemical Aspects of Ischemic Injury 43
2.1 Introduction 43
2.2 Ischemic Injury-Mediated Alterations in Glycerophospholipid Metabolism 47
2.3 Ischemic Injury-Mediated Alterations in Protein Metabolism 52
2.4 Ischemic Injury-Mediated Alterations in Nucleic Acid Metabolism 55
2.5 Ischemic Injury-Mediated Alterations in Enzymic Activities 58
2.6 Ischemic Injury-Mediated Alterations in Nuclear Transcription Factor-B (NF-B) 59
2.7 Ischemic Injury-Mediated Alterations in Genes 61
2.8 Ischemic Injury-Mediated Alterations in Cytokines and Chemokines 64
2.9 Ischemic Injury-Mediated Alterations in Heat Shock Proteins 66
2.10 Ischemic Injury-Mediated Alterations in Adehesion Molecules 67
2.11 Ischemic Injury-Mediated Alterations in Apoptosis-Inducing Factor 68
2.12 Ischemic Injury-Mediated Alterations in Na /Ca 2 Exchanger 69
2.13 Mechanism of Neurodegeneration in Ischemia/Reperfusion Injury 71
2.14 Conclusion 73
References 74
3 Potential Neuroprotective Strategies for Ischemic Injury 82
3.1 Introduction 82
3.2 Potential Treatment Strategies for Ischemic Injuries 83
3.2.1 N-Methyl-d-Aspartate Receptor Antagonists and Stroke Therapy 88
3.2.2 Calcium Channel Blockers and Stroke Therapy 89
3.2.3 Free Radical Scavengers and Stroke Therapy 89
3.2.4 GM1 Ganglioside and Stroke Therapy 93
3.2.5 Statins and Stroke Therapy 94
3.2.6 w-3 Fatty Acids and Stroke 95
3.2.7 Citicoline (CDP-Choline) and Stroke Therapy 97
3.2.8 Peroxisome Proliferator-Activated Receptor -Agonists and Stroke 99
3.2.9 Hypoxia-Inducible Factor 1 and Stroke Therapy 100
3.2.10 Vaccine and Stroke Therapy 101
3.2.11 Pipeline Developments on Drugs for Stroke Therapy 102
3.2.12 Intracellular Cell Therapy in Stroke 104
3.3 Mechanism of Neuroprotection in Ischemic Injury 105
3.3.1 Prevention of Stroke Through the Modulation of Risk Factors 107
3.3.2 Selection of Diet and Stroke 107
3.3.3 Physical Exercise and Stroke 110
3.3.4 Transcranial Magnetic Stimulation and Stroke Rehabilitation 111
3.3.5 Occupational Therapy and Rehabilitation After Stroke 112
3.4 Conclusion 113
References 114
4 Neurochemical Aspects of Spinal Cord Injury 122
4.1 Introduction 122
4.2 Regeneration and Neuritogenesis in SCI 124
4.3 Necrosis and Apoptosis in SCI 126
4.4 Contribution of Excitotoxicity in Spinal Cord Injury 127
4.5 Enzymic Activities in Spinal Cord Injury 129
4.5.1 Activation of PLA 2 in Spinal Cord Injury 129
4.5.2 Activation of COX-2 in Spinal Cord Injury 131
4.5.3 Activation of NOS in Spinal Cord Injury 132
4.5.4 Activation of Calcineurin in Spinal Cord Injury 134
4.5.5 Activation of Matrix Metalloproteinases in Spinal Cord Injury 134
4.5.6 Activation of Poly (ADP-Ribose) Polymerase in Spinal Cord Injury 136
4.5.7 Activation of RhoA and RhoB in Spinal Cord Injury 137
4.5.8 Activation of Caspases in Spinal Cord Injury 137
4.5.9 Activation of Calpains and Other Proteases in Spinal Cord Injury 138
4.6 Activation of Cytokines and Chemokines in Spinal Cord Injury 139
4.7 Fas/CD95 ReceptorLigand System in Spinal Cord Injury 141
4.8 Activation of Transcription Factors in Spinal Cord Injury 141
4.8.1 NF-plus1fillB 0 in Spinal Cord Injury 142
4.8.2 Peroxisome Proliferator-Activated Receptor in Spinal Cord Injury 143
4.8.3 STAT in Spinal Cord Injury 143
4.8.4 AP-1 in Spinal Cord Injury 144
4.9 Gene Transcription in Spinal Cord Injury 145
4.10 Mitochondrial Permeability Transition in Spinal Cord Injury 145
4.11 Heat Shock Proteins in Spinal Cord Injury 147
4.12 Growth Factors in Spinal Cord Injury 148
4.13 Other Neurochemical Changes in Spinal Cord Injury 150
4.14 Neuropathic Pain in SCI 151
4.15 Contribution of Oxidative Stress in Spinal Cord Injury 152
4.16 Inflammation in Spinal Cord Injury 153
4.17 Interactions Among Excitotoxicity, Oxidative Stress, and Inflammation in Spinal Cord Injury 155
4.18 Conclusion 156
References 157
5 Potential Neuroprotective Strategies for Experimental Spinal Cord Injury 165
5.1 Introduction 165
5.2 Metalloproteinases and Glial Scar Formation 166
5.3 Other Inhibitory Molecules Contributing to Axonal Growth Inhibition 166
5.4 Neuroprotective Strategies 170
5.4.1 Methylprednisolone and SCI 171
5.4.2 GM1 Ganglioside and SCI 174
5.4.3 Tirilazad Mesylate and SCI 175
5.4.4 Inhibitors of Calpains, Nitric Oxide Synthase, and PLA2 and SCI 176
5.4.5 Minocycline and SCI 179
5.4.6 Thyrotropin-Releasing Hormone and SCI 181
5.4.7 Dantrolene and SCI 181
5.4.8 -3 Fatty Acids and SCI 182
5.4.9 Polyethylene Glycol and SCI 182
5.4.10 Opioid Receptor Antagonists, Glutamate Receptor Antagonists, and Calcium Channel Blockers in SCI 183
5.4.11 Growth Factors and SCI 184
5.5 Regeneration and SCI 184
5.5.1 Stem/Progenitor Cell Transplants 185
5.5.2 Human Umbilical Cord Blood Stem Cells Transplants 186
5.6 Rehabilitation and SCI 187
5.7 Conclusion 188
References 188
6 Neurochemical Aspects of Traumatic Brain Injury 196
6.1 Introduction 196
6.2 TBI-Mediated Alterations in Glutamate and Calcium Levels 199
6.3 TBI-Mediated Alterations in Cytokines 200
6.4 TBI-Mediated Alterations in Chemokines 201
6.5 TBI-Mediated Alterations in Enzymic Activities 202
6.5.1 PLA2 and DAG/PLC Pathway in TBI 203
6.5.2 Cyclooxygenases (COX) and Lipoxygenases (LOX) in TBI 204
6.5.3 Calpain Activity in TBI 205
6.5.4 Caspases in TBI 205
6.5.5 Nitric Oxide Synthase in TBI 206
6.5.6 Kinases in TBI 207
6.5.7 Matrix Metalloproteinases (MMPs) in TBI 209
6.5.8 Calcineurin in TBI 209
6.5.9 Other Enzymes in TBI 210
6.6 TBI-Mediated Alterations in Cytoskeletal Protein 210
6.7 TBI-Mediated Alterations in Transcription Factors 211
6.7.1 Nuclear Factor Kappa B (NF-kB) in TBI 211
6.7.2 Signal Transducers and Activators of Transcription (STATs) in TBI 213
6.7.3 Nuclear Factor E2-Related Factor 2 in TBI 213
6.7.4 AP-1 Transcription Factor in TBI 214
6.7.5 CCAAT/Enhancer-Binding Protein (C/EBP) in TBI 214
6.8 TBI-Mediated Alterations in Gene Expression 215
6.9 TBI-Mediated Alterations in Adhesion Molecules 217
6.10 TBI-Mediated Alterations in Neurotrophic Factors 217
6.11 TBI-Mediated Alterations in Complement System 218
6.12 TBI Mediators Alterations in Endocannabinoids 219
6.13 TBI-Mediated Changes in Hydroxycholesterols 219
6.14 TBI and Apoptotic Cell Death 220
6.15 Molecular Mechanism of Neurodegeneration in TBI 221
6.16 Conclusion 223
References 223
7 Potential Neuroprotective Strategies for Traumatic Brain Injury 232
7.1 Introduction 232
7.2 Regeneration and Neuritogenesis in TBI 233
7.3 Potential Neuroprotective Strategies for TBI 234
7.3.1 Statins and TBI 235
7.3.2 Progesterone and TBI 238
7.3.3 Erythropoietin and TBI 242
7.3.4 Minocycline and TBI 244
7.3.5 PPAR Agonist and TBI 245
7.3.6 Endocannabinoids and TBI 247
7.3.7 Thyrotropin-Releasing Hormone (TRH) and TBI 250
7.3.8 Citicoline (CDP-Choline) and TBI 250
7.3.9 w-3 Fatty Acids and TBI 251
7.3.10 Hypothermia and TBI 252
7.4 Cell Therapy and TBI 253
7.5 Conclusion 254
References 254
8 Neurochemical Aspects of Neurodegenerative Diseases 262
8.1 Introduction 262
8.2 Factors and Molecular Mechanisms that Modulate Neurodegeneration in Neurodegenerative Diseases 264
8.3 Neurochemical Aspects of Alzheimer Disease 267
8.3.1 Lipids in AD 269
8.3.2 Protein in AD 272
8.3.3 Nucleic Acid in AD 277
8.3.4 Transcription Factors in AD 278
8.3.5 Gene Expression in AD 279
8.3.6 Neurotrophins in AD 280
8.3.7 Insulin and Insulin-Like Growth Factor in AD 281
8.4 Neurochemical Aspects of Parkinson Disease 282
8.4.1 Lipids in PD 283
8.4.2 Proteins in PD 285
8.4.3 Nucleic Acids in PD 287
8.4.4 Transcription Factors in PD 288
8.4.5 Gene Expression in PD 289
8.4.6 Neurotrophins in PD 290
8.5 Neurochemical Aspects of Amyotropic Lateral Sclerosis 291
8.5.1 Lipids in ALS 293
8.5.2 Proteins in ALS 294
8.5.3 Nucleic Acids in ALS 295
8.5.4 Transcription Factors in ALS 296
8.5.5 Gene Expression in ALS 296
8.5.6 Neurotrophins in ALS 297
8.6 Neurochemical Aspects of Huntington Disease 298
8.6.1 Lipids in HD 299
8.6.2 Proteins in HD 300
8.6.3 Nucleic Acids in HD 302
8.6.4 Transcription Factors in HD 302
8.6.5 Gene Expression in HD 303
8.6.6 Neurotrophins in HD 304
8.7 Neurochemical Aspects of Prion Diseases 305
8.7.1 Lipids in Prion Diseases 307
8.7.2 Proteins in Prion Diseases 309
8.7.3 Nucleic Acids in Prion Diseases 310
8.7.4 Transcription Factors in Prion Diseases 310
8.7.5 Gene Expression in Prion Diseases 310
8.7.6 Neurotrophins in Prion Diseases 311
8.8 Complement System Changes and Neurodegenerative Diseases 312
8.9 Apoptotic and Necrotic Cell Death and Autophagy in Neurodegenerative Diseases 313
8.10 Mechanisms of Neurodegeneration in Neurodegenerative Diseases 316
8.11 Conclusion 320
References 321
9 Potential Therapeutic Strategies for Neurodegenerative Diseases 338
9.1 Introduction 338
9.2 Factors Influencing the Onset of Neurodegenerative Diseases 339
9.2.1 Genetic and Environmental Factors 340
9.2.2 Lifestyle and Neurodegenerative Diseases 341
9.2.3 Diet and Neurodegenerative Diseases 343
9.3 Therapeutic Approaches for AD 346
9.3.1 Cholinergic Strategies 346
9.3.2 Antioxidant, Anti-inflammatory, and Antiexcitotoxic Strategies in AD 349
9.3.3 Stabilization of Mitochondrial Dynamics and AD 350
9.3.4 Statins and AD Treatment 352
9.3.5 Memantine and AD Treatment 354
9.3.6 Secretase Inhibitors and AD Treatment 356
9.3.7 PPAR Agonists and AD Treatment 357
9.3.8 Neurotrophins and AD Treatment 359
9.3.9 w-3 Fatty Acids and AD Treatment 360
9.3.10 Immunization Therapy in AD 362
9.3.11 AL-108 or NAP Therapy in AD 363
9.4 Therapeutic Approaches for PD 363
9.4.1 Dopaminergic Strategies in PD 364
9.4.2 Antioxidant, Anti-inflammatory, and Antiexcitotoxic Strategies in PD 364
9.4.3 Stabilization of Mitochondrial Dynamics in PD 365
9.4.4 Statins and PD Treatment 367
9.4.5 Memantine and PD Treatment 368
9.4.6 PPAR Agonists and PD Treatment 369
9.4.7 Neurotrophins and PD Treatment 370
9.4.8 w-3 Polyunsaturated Fatty Acids and PD Treatment 370
9.5 Therapeutic Approaches for ALS 371
9.5.1 Riluzole and Memantine and ALS Treatment 372
9.5.2 Antioxidant Strategies and ALS Treatment 373
9.5.3 Stabilization of Mitochondrial Dynamics and ALS Treatment 373
9.5.4 Neurotrophins and ALS Treatment 374
9.5.5 w-3 Fatty Acids and ALS Treatment 375
9.5.6 Immunotherapy and ALS Treatment 375
9.6 Therapeutic Approaches for HD 375
9.6.1 Gene Silencing and HD Treatment 376
9.6.2 Enhancement of Protein Degradation and HD Treatment 376
9.6.3 Inhibition of Aggregation and HD Treatment 377
9.6.4 Creatine and Other Antioxidants and HD Treatment 377
9.6.5 Minocycline and HD Treatment 378
9.6.6 w-3 Fatty Acids and HD Treatment 378
9.7 Therapeutic Approaches for Prion Diseases 378
9.7.1 Pentosan Polysulfate for the Treatment of Prion Diseases 379
9.7.2 Quinacrine for the Treatment of Prion Diseases 379
9.7.3 Glimepiride for the Treatment of Prion Diseases 381
9.7.4 Vaccine for the Treatment of Prion Diseases 381
9.8 Conclusion 382
References 383
10 Perspective and Direction for Future Developments on Neurotraumatic and Neurodegenerative Diseases 396
10.1 Introduction 396
10.2 Factors Contributing to Increased Frequency of Neurotraumatic and Neurodegenerative Diseases 398
10.2.1 Diet and Frequency of Occurrence of Neurotraumatic and Neurodegenerative Diseases 399
10.2.2 Detection of Neurotraumatic and Neurodegenerative Diseases 400
10.3 Proteomics and Lipidomics in Neurotraumatic and Neurodegenerative Diseases 401
10.4 Vaccines for the Treatment of Neurotraumatic and Neurodegenerative Diseases 402
10.5 Reasons for the Failure of Treatment in Neurotraumatic and Neurodegenerative Diseases 403
10.6 Future Studies on the Treatment of Neurotraumatic and Neurodegenerative Diseases 404
10.7 Conclusion 406
References 407
Index 411
| Erscheint lt. Verlag | 2.9.2010 |
|---|---|
| Zusatzinfo | XXIII, 401 p. |
| Verlagsort | New York |
| Sprache | englisch |
| Themenwelt | Medizin / Pharmazie ► Medizinische Fachgebiete ► Neurologie |
| Studium ► 1. Studienabschnitt (Vorklinik) ► Biochemie / Molekularbiologie | |
| Naturwissenschaften ► Biologie ► Humanbiologie | |
| Naturwissenschaften ► Biologie ► Zoologie | |
| Schlagworte | acute neural trauma • Alzheimer • excitotoxicity • Neurodegeneration • neurons • Parkinson |
| ISBN-10 | 1-4419-6652-8 / 1441966528 |
| ISBN-13 | 978-1-4419-6652-0 / 9781441966520 |
| Haben Sie eine Frage zum Produkt? |
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