Protein Misfolding in Neurodegenerative Diseases: Mechanisms and Therapeutic StrategiesRobert D. E. Sewell CRC Press, 3 дек. 2007 г. - Всего страниц: 592 Current research suggests that neurodegenerative diseases such as Alzheimer's, Parkinson's, Huntington's, and Creutzfeldt-Jacob may be linked to disorders in protein shape referred to as protein misfolding. Continued study in this area could lead to promising advances in future treatment of these diseases. This groundbreaking text describes the latest findings regarding protein misfolding in the context of it being a marker, and perhaps a cause, in neurodegenerative diseases. Comprehensive coverage includes the diverse biochemical targets/markers for each disease, the currently limited success of drug therapies, and the cutting-edge research that could lead to more promising treatments. |
Содержание
| 1 | |
Chapter 2 Alzheimers Disease | 69 |
Chapter 3 Improving Cholinergic Transmission | 95 |
Chapter 4 Reduction in Plaque Formation | 145 |
Chapter 5 Carbonic Anhydrase Activators as Potential AntiAlzheimers Disease Agents | 265 |
Chapter 6 Detection and Reduction of Neurofibrillary Lesions | 289 |
Pathogenic or Protective? | 327 |
Chapter 8 Enhancement of Brain Retinoic Acid Levels | 337 |
Chapter 10 Restoring Dopamine Levels | 415 |
Chapter 11 Huntingtons Disease | 449 |
Chapter 12 Amyotrophic Lateral Sclerosis Motor Neuron Disease | 479 |
Chapter 13 Transmissible Spongiform Encephalopathies | 517 |
Chapter 14 Overview | 547 |
Index | 557 |
Back cover | 571 |
What Is It? What Causes It? And How Can It Be Cured? | 381 |
Другие издания - Просмотреть все
Protein Misfolding in Neurodegenerative Diseases: Mechanisms and Therapeutic ... Robert D. E. Sewell Недоступно для просмотра - 2019 |
Protein Misfolding in Neurodegenerative Diseases: Mechanisms and Therapeutic ... Robert D. E. Sewell Недоступно для просмотра - 2007 |
Часто встречающиеся слова и выражения
a-synuclein Abeta Academy of Sciences acetylcholinesterase activity Alzheimer disease Alzheimer’s disease amino acid amyloid fibrils amyloid-b amyloidosis amyotrophic lateral sclerosis associated b-amyloid beta-amyloid binding Biological Chemistry brain cell cellular cholesterol clinical cognitive compounds decreased dementia deposition disorders donepezil dopamine dopaminergic drug effects enzyme expression factor filament formation function g-secretase gene Genetics human huntingtin Huntington’s disease increased inhibition inhibitors interaction isoforms Journal of Biological Journal of Neuroscience kinase levels levodopa ligands mechanism Medicinal Chemistry membrane metabolism microtubule modulate Molecular molecules motor neuron mouse model mutations National Academy neurodegenerative Neurology NSAIDs oligomers onset oxidative Parkinson’s disease pathology pathway patients peptide Pharmacology phenotype phosphorylation plaques potential prion disease protein aggregation protein folding PrPSc rasagiline receptor Research retinoic acid retinoid role SOD1 soluble specific statins structure studies substrate Supuran synthesis target tau protein therapeutic therapy tissue toxicity transgenic transgenic mice treatment vitro vivo
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