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دسته بندی: عصب شناسی ویرایش: نویسندگان: Lars P. Klimaschewski سری: ISBN (شابک) : 3662663686, 9783662663684 ناشر: Springer سال نشر: 2022 تعداد صفحات: 163 زبان: English فرمت فایل : PDF (درصورت درخواست کاربر به PDF، EPUB یا AZW3 تبدیل می شود) حجم فایل: 3 مگابایت
در صورت تبدیل فایل کتاب Parkinson's and Alzheimer's Today: About Neurodegeneration and its Therapy به فرمت های PDF، EPUB، AZW3، MOBI و یا DJVU می توانید به پشتیبان اطلاع دهید تا فایل مورد نظر را تبدیل نمایند.
توجه داشته باشید کتاب پارکینسون و آلزایمر امروز: درباره تخریب عصبی و درمان آن نسخه زبان اصلی می باشد و کتاب ترجمه شده به فارسی نمی باشد. وبسایت اینترنشنال لایبرری ارائه دهنده کتاب های زبان اصلی می باشد و هیچ گونه کتاب ترجمه شده یا نوشته شده به فارسی را ارائه نمی دهد.
Preface Contents 1 Introduction to Brain Development: Why do We Need so Many Nerve Cells? 1.1 Neurons and Glia in the Central Nervous System 1.2 What Happens During Brain Development? 1.3 Evolutionarily Old Brain Parts are Simpler in Structure than the Neocortex 1.4 What Distinguishes the Left from the Right Brain? 1.5 Brain Development in Childhood and Adolescence 1.6 The Child’s Brain is Enormously Plastic and can Still Heal 1.7 Is a Large Brain “Smarter” than a Small One? 1.8 Absolute and Relative Brain Weight 1.9 With the Second Evolutionary Leap, Our Brain Reaches its Maximum Size 1.10 Neural Stem Cells Remain Capable of Dividing for a Long Time 1.11 The Frontal Lobe is Especially Important for Higher Brain Functions 1.12 The Prefrontal Cortex Encodes Human Specific Properties 1.13 Brain Performance in Comparison Further Reading 2 Aging and Neurodegenerative Diseases: Why do Nerve Cells Die? 2.1 The Normal Aging Process 2.1.1 Mechanisms of Cellular Aging DNA Telomeres Determine the Number of Cell Divisions Aging Cells Maintain a Chronic Inflammation The Importance of Protein Homeostasis for Cellular Aging Self-cleaning of Nerve Cells Two Sides of a Coin: Oxygen Radicals Endogenous Radical Scavengers Protect Our Nerve Cells Chronic Inflammatory Processes in the Brain 2.1.2 Neuronal Cell Death How do neurons die? 2.1.3 Blood Supply of the Aging Brain Barrier Disorders are Not Uncommon in the Elderly 2.2 Parkinson’s Disease 2.2.1 General Pathomechanisms The Problem with Parkinson’s Begins in the Lower Brainstem 2.2.2 Special Morphology of Affected Neurons Special Requirements for Highly Branched Neurons Many Amine-releasing Neurons are Constantly Active and Therefore More Easily Stressed 2.2.3 Specific Causes of Parkinson’s Disease 2.2.4 Alpha-synuclein: A Key Protein in Parkinson’s Disease Fibrils Are More Dangerous Than Aggregates Aggregates Are Not Only Found in Nerve Cells 2.2.5 The Prion Theory of Parkinson’s Disease Cranial Nerves Transport Pathological Proteins into the Brain The Difficulties of a Clear Pathogenesis of Parkinson’s Disease 2.3 Dementia and Alzheimer’s Disease 2.3.1 How Does Alzheimer’s Disease Manifest Itself? 2.3.2 General Pathomechanisms The Amyloid Pathology The Many Effects of Aβ Peptides 2.3.3 The Disturbed Protein Homeostasis in Alzheimer’s Disease 2.3.4 Tau Pathology Pathological Effects of p-tau and Aβ Episodic Memory is Already Impaired in the Early Stage of Alzheimer\'s 2.3.5 The Prion Theory in Alzheimer’s Disease The Relevance of Cerebrospinal Fluid Drainage for Neurodegeneration 2.4 Inflammatory Components of Alzheimer’s and Parkinson’s Disease 2.5 Viral Infections in Neurodegenerative Diseases Further Reading 3 Saving or Replacing Nerve Cells: Which Strategy is More Successful? 3.1 Parkinson’s Disease 3.1.1 Pharmacological Therapy 3.1.2 Surgical and physical therapy 3.1.3 Therapy with Neurotrophic Factors 3.1.4 Therapy with Antisense Oligonucleotides 3.1.5 Alpha-synuclein Aggregation Inhibitors and Specific Immunotherapy 3.1.6 Stem Cell Therapy 3.1.7 Other Causal Therapeutic Approaches 3.2 Dementia and Alzheimer’s Disease 3.2.1 Cholinergica 3.2.2 Therapy with Secretase Inhibitors 3.2.3 Therapy with Neurotrophic Factors 3.2.4 Immunotherapy 3.2.5 Stem Cell Therapy 3.2.6 Other Causal Therapeutic Approaches 3.2.7 Symptomatic Therapy 3.2.8 Which Measures Promise the most Success? 3.3 Diagnosis and Therapy of Neuronal Degeneration—quo vadis? Further Reading Glossary