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The Science of the Brain Function, Dysfunction and Disease

Συγγραφείς: Ari Rappoport
ISBN: 9780443450082
Εκδότης: Academic Press
Σελίδες: 358
Διαστάσεις: 15 x 22 cm
Έτος Έκδοσης: 2025

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The Science of the Brain: Function, Dysfunction and Disease is an innovative exploration into the complex interplay between brain functionality and various neurological disorders, meticulously compiled by a world-renowned researcher. This groundbreaking book presents a comprehensive analysis, offering the first complete theories for eleven major brain disorders, including Alzheimer’s, schizophrenia, and autism spectrum disorder, among others. Each chapter delves into a unique theoretical framework, from lipid raft theories to sympathetic nervous system impacts, all while proposing potential treatment targets grounded in established scientific data. In addition to two chapters that lay the groundwork for understanding brain adaptability and anatomy, other chapters independently dissect each disorder, revealing fresh insights that promise to invigorate research and clinical application. This essential resource not only serves neuroscientists and clinicians seeking a deeper understanding of brain disorders but also invites entrepreneurs interested in novel therapeutic avenues. With its rich references and pioneering theories, this book is poised to become indispensable to students, researchers and clinicians, paving the way for future discoveries in brain health and disease management.

Identifies connections between brain functionality and specific disorders, revealing previously unexplored therapeutic avenues
Challenges existing paradigms in neuroscience by presenting the first comprehensive theories for a range of neurological and psychiatric conditions
Utilizes detailed references and robust scientific data to support groundbreaking claims and methodologies

CONTENTS

Chapter 1: A CRH2-ACTH theory of autism spectrum disorder
1.1. Introduction
1.2. Theory
1.2.1. Urocortins (UCNs)
1.2.2. Steroids (STRDs)
1.2.3. Explaining ASD symptoms and properties
1.3. Evidence
1.3.1. Stress, CRH, ACTH
1.3.2. Anatomical growth
1.3.3. Growth agents & pathways
1.3.4. Sex steroids
1.3.5. Oxytocin
1.3.6. Food intake
1.4. Treatment
1.4.1. Detection
1.4.2. Preventive treatment
1.4.3. Symptomatic treatment
1.5. Discussion
List of abbreviations
Chapter 2: A CRH2-CRH1 theory of anorexia and bulimia
2.1. Introduction
2.2. Theory
2.2.1. CRH, CRH1, CRH2, serotonin
2.2.2. Anorexia nervosa (AN)
2.2.3. Bulimia nervosa
2.3. Evidence
2.4. Treatment
2.5. Discussion
List of abbreviations
Chapter 3: A polyunsaturated fatty acid (PUFA) theory of schizophrenia
3.1. Introduction
3.2. PUFA theory of schizophrenia (P*SZ)
3.3. PUFAs and PUFA derivatives in health
3.4. PUFAs and PUFA derivatives and stress
3.5. Evidence for P*SZ
3.5.1. PUFAs
3.5.2. Immunity and pain
3.5.3. ECB system
3.5.4. Hyperexcitability: neuromodulators, hormones, neurotransmitters
3.5.5. Coordinated network activity
3.5.6. Summary
3.6. Treatment
3.7. Discussion
List of abbreviations
Chapter 4: A dynorphin theory of depression and bipolar disorder
4.1. Introduction
4.2. Stress responses and MDD
4.3. A theory of opioids and survival responses
4.4. A theory of depression and bipolar disorder
4.5. Evidence
4.6. Treatment
4.7. Discussion
List of abbreviations
Chapter 5: A CRH-HCN theory of obsessive-compulsive disorder (OCD)
5.1. Theory
5.2. Treatment
5.3. Key references
Chapter 6: A KATP channel theory of attention-deficit hyperactivity disorder
6.1. Theory
6.2. Treatment
6.3. Evidence and references
Chapter 7: A sympathetic nervous system theory of migraine
7.1. Introduction
7.2. Theory
7.2.1. SNS and BRRs
7.2.2. TRPV1, CGRP
7.2.3. Migraine
7.3. Evidence
7.3.1. Basal state
7.3.2. Acute headache state
7.4. Treatment
7.5. Discussion
List of abbreviations
Chapter 8: A ceramide theory of multiple sclerosis
8.1. Introduction
8.2. Theory
8.2.1. Background
8.2.2. Multiple sclerosis
8.3. Evidence
8.4. Treatment
8.5. Discussion
List of abbreviations
Chapter 9: A calcium channel α2δ subunit theory of amyotrophic lateral sclerosis and frontotemporal dementia
9.1. Introduction
9.2. Voltage-gated calcium channels (VGCCs)
9.3. Proposed calcium & a2d impairment in ALS
9.3.1. Motivation
9.3.2. Calcium part of the theory
9.3.3. a2d part of the theory
9.4. ALS evidence
9.4.1. Calcium
9.4.2. Explanatory power for ALS facts
9.4.3. a2d
9.4.4. Insulin
9.5. Autoimmunity
9.6. Frontotemporal dementia (FTD)
9.7. Discussion
Chapter 10: A galactose theory of Parkinson's disease
10.1. Introduction
10.2. T*PD theory of PD
10.3. Evidence
10.3.1. Gut bacteria, mucin
10.3.2. Galactose
10.3.3. Glucose
10.3.4. Oxidative stress
10.3.5. Sympathetic nervous system
10.3.6. Risk & protective factors
10.4. Treatment
10.5. Discussion
List of abbreviations
Chapter 11: A lipid-raft theory of Alzheimer's disease
11.1. Introduction
11.1.1. Overview of the theory of adaptive response plasticity
11.1.2. Overview of the lipid-raft theory of Alzheimer's disease
11.2. The theory of adaptive response plasticity
11.2.1. Double-edged plasticity
11.2.2. Long-term potentiation and long-term depression
11.2.3. The steady state
11.2.4. Candidate generation
11.2.5. Cholesterol, apolipoprotein E, and lipid rafts
11.2.6. Competition resolution: winners and losers
11.2.7. Summary
11.3. The lipid-raft theory of Alzheimer's disease
11.3.1. Mechanisms underlying symptoms and pathology
11.3.2. Chronicity
11.3.3. Cholesterol and amyloid β
11.3.4. Tau
11.3.5. Core cause
11.3.6. Autosomal dominant Alzheimer's disease
11.4. Evidence
11.4.1. Lipid rafts
11.4.2. Cholesterol
11.4.3. Polyunsaturated fatty acids
11.4.4. Plasticity agents
11.4.5. Synapses
11.4.6. Brain areas
11.4.7. Genetics
11.4.8. Other diseases
11.5. Risk and protective factors
11.5.1. Viral infections
11.5.2. Traumatic brain injury
11.5.3. Diabetes and obesity
11.5.4. Vascular impairment
11.5.5. Immunity
11.5.6. Stress
11.5.7. Smoking
11.5.8. Education and bilingualism
11.5.9. Exercise
11.6. Discussion
11.6.1. Related theories
11.6.2. The theory of adaptive response plasticity
11.6.3. Sleep
11.6.4. Neurogenesis
11.6.5. Dementia
11.6.6. Theory predictions
Chapter 12: The brain's adaptive response process: function and anatomy
12.1. Explaining the brain
12.2. The adaptive response process (ARP)
12.2.1. Response selection
12.2.2. Response release: ARAR circuits
12.2.3. Novel vs. Automated (learned) responses
12.2.4. Agents
12.3. IINs: competition resolution (cres) & execution
12.4. Goals and predictions
12.5. The basal ganglia and the cerebellum
12.6. Hierarchical sequences (HSEQs)
12.7. Additional evidence
12.8. Discussion
12.8.1. The explanatory power and biological logic of the theory
12.8.2. Function and anatomy
12.8.3. Other theories; contribution
12.8.4. Action execution, observation, imagery
12.8.5. Language
12.8.6. Fully explaining the brain
12.8.7. Consciousness and emotions
Author's comment
Chapter 13: The brain's ‘Allow, Restrain, Amplify, Respond’ (ARAR) architecture
13.1. Introduction
13.2. The D1 ARAR circuit
13.3. The D2 circuit: automated (learned) responses
13.3.1. The circuit
13.3.2. Problems with the standard D2 account
13.3.3. Evidence supporting a learned movement role of the D2 path
13.4. The extended amygdala ARAR circuit
13.5. The habenula ARAR circuit
13.6. The superior colliculus ARAR circuit
13.7. The hippocampus ARAR circuit
13.8. The cerebellum ARAR circuit
13.9. Discussion
Chapter 14: A comprehensive biological theory of sleep
14.1. Introduction
14.2. Theory overview
14.3. Wake activity
14.4. Homeostasis and its restoration
14.5. NREM sleep
14.6. REM sleep
14.7. Consciousness
14.8. Memory and plasticity
14.9. Anesthesia
14.10. Discussion
14.11. Conclusio