Neurodegeneration and Alzheimer's Disease

Name: Neurodegeneration and Alzheimer's Disease | The Role of Diabetes, Genetics, Hormones, and Lifestyle
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The Role of Diabetes, Genetics, Hormones, and Lifestyle

Ralph N. Martins Charles S. Brennan Binosha Fernando Margaret A. Brennan Stephanie J. Fuller(Herausgeber*in)

Wiley (Verlag)

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Erschienen am 26. April 2019

544 Seiten

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Beschreibung

Understanding the impact of diet, exercise, genetics, and hormones on the risk and development of Alzheimer's and other neurogenerative diseases

Diet is widely known to impact on neurological function. Nevertheless, academic texts discussing this relationship are relatively few in number. This book therefore fills an important gap in the current literature. Opening with an overview of neurodegenerative diseases, particularly Alzheimer's disease, the text then focuses on explaining the means by which glycemic control and lipid metabolism - and associated nutritional and lifestyle variables - may factor into such disorders' prevention and treatment.

An international group of experts in the fields of food science and neurodegeneration have contributed chapters that examine Alzheimer's disease within a broad range of contexts. Offering dietary, genetic, and hormonal perspectives, the authors explore topics ranging from sugar consumption to digestive fermentation, and Alzheimer's disease animal models to the cognition-enhancing effects of physical exercise. Also included are overviews of the latest research into current and developing methods of treatment and diagnosis, as well as differential diagnostics. This groundbreaking book:

* Explores how glucose metabolism, insulin resistance, lipid metabolism, and high intake of refined carbohydrates are linked to Alzheimer's disease

* Discusses how genetic makeup can impact risk of Alzheimer's and Parkinson's disease

* Examines cognitive changes in neurodegeneration, lists current tests for determining cognitive impairment, and provides information concerning differential diagnosis

* Discusses potential advantages of increasing antioxidant and micronutrient intake

* Reviews hormonal influences on neurodegeneration

* Examines the links between protein intake and Alzheimer's disease.

Neurodegeneration and Alzheimer's Disease is an essential resource for researchers, medical practitioners, dietitians, and students with an interest in neurological diseases and their diagnosis and risk factors, as well as diet-related conditions such as diabetes and obesity. Lifestyle and diet influence neurodegeneration risk, and a better understanding of this evidence amongst health professionals will hopefully lead to greater public awareness of how to reduce the likelihood of these widespread conditions.

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Inhalt

Cover
Title Page
Copyright
Contents
List of Contributors
Chapter 1 Current Understanding of Alzheimer's Disease and Other Neurodegenerative Diseases, and the Potential Role of Diet and Lifestyle in Reducing the Risks of Alzheimer's Disease and Cognitive Decline
References
Chapter 2 Alzheimer's Disease and Other Neurodegenerative Diseases
2.1 Introduction
2.2 Alzheimer's Disease
2.2.1 Pathology
2.2.2 Symptoms
2.2.3 Incidence
2.2.4 Onset and Risk Factors
2.2.5 Treatment
2.2.6 Potential for AD Prevention
2.3 Frontotemporal Lobe Dementia
2.3.1 Neuropathology and Causes
2.3.2 Treatment
2.3.3 Diagnosis and Clinical Overlap with Other Diseases
2.4 Vascular Dementia
2.4.1 Symptoms and Diagnosis
2.4.2 Causes and Risk Factors
2.4.3 Prevention and Treatment
2.4.4 Dementia with Lewy Bodies
2.4.5 Causes
2.4.6 Symptoms
2.4.7 Diagnosis of DLB
2.4.7.1 Clinical Approach to Dementias
2.5 Parkinson's Disease
2.5.1 Onset
2.5.2 Causes and Risk Factors
2.5.3 Incidence
2.5.4 Pathology
2.5.5 Treatment
2.6 Huntington's Disease
2.6.1 Genetics of the Disease
2.6.2 Incidence and Prevalence
2.6.3 Pathology
2.6.4 Treatment
2.7 Motor Neuron Diseases
2.7.1 Amyotrophic Lateral Sclerosis
2.7.2 Spinal Muscular Atrophy
2.7.3 Hereditary Spastic Paraplegia
2.7.4 Onset of MND and Differential Diagnosis
2.7.5 Incidence, Causes, and Risk Factors
2.7.6 Pathology
2.7.7 Treatment
2.8 Prion Diseases
2.8.1 Causes
2.8.2 Symptoms and Diagnosis
2.8.3 Treatment
2.8.4 Differential Diagnosis of the Various Types of Dementia
2.8.5 DLB Treatment
2.9 Summary
References
Chapter 3 Current and Developing Methods for Diagnosing Alzheimer's Disease
3.1 Introduction
3.2 Classical Post-Mortem Diagnosis
3.2.1 Plaques
3.2.2 Neurofibrillary Tangles (NFT)
3.2.3 Cerebral Amyloid Angiopathy (CAA)
3.2.4 Glial Responses
3.2.5 Brain Shrinkage
3.2.6 Loss of Synapses and Neurons
3.3 Clinical Diagnosis
3.3.1 Initial Assessment/Screening Tools
3.3.1.1 Mini-Mental State Examination (MMSE)
3.3.1.2 Montreal Cognitive Assessment (MoCA)
3.3.1.3 Clinical Dementia Rating (CDR)
3.3.1.4 Clock Drawing
3.3.1.5 Seven-Minute Screen
3.3.1.6 Alzheimer's Disease Assessment Scale (ADAS-Cog)
3.3.1.7 Psychogeriatric Assessment Scales (PAS)
3.3.1.8 Dementia Rating Scale (DRS)
3.3.1.9 Mini-Cog
3.3.1.10 Rowland Universal Dementia Assessment Scale (RUDAS)
3.3.1.11 The Consortium to Establish a Registry for Alzheimer's Disease (CERAD) Neuropsychological Battery (nb) and Other Tests
3.4 Brain Imaging in the Diagnosis of Alzheimer's Disease and Other Dementias
3.4.1 Imaging Tests in AD Diagnosis: Established Tests
3.4.1.1 Computed Tomography (CT)
3.4.1.2 Electroencephalography (EEG)
3.4.1.3 Magnetic Resonance Imaging (MRI), for the Assessment of Morphological Changes, and the Detection of Stroke
3.4.1.4 Positron Emission Tomography (PET)
3.4.1.5 FDG-PET
3.4.2 Imaging Tests in AD Diagnosis: More Recently Developed Tests
3.4.2.1 MRI for Measuring Regional Blood Flow
3.4.2.2 Single Photon Emission Computed Tomography (SPECT) Scan
3.4.2.3 PiB-PET
3.4.3 The Rapidly Evolving Diagnostic Criteria
3.4.4 CSF Biomarkers of AD
3.4.4.1 A&rmbeta
, Tau, and A&rmbeta
PP-Related Biomarkers
3.4.4.2 Other Potential CSF Protein Biomarkers
3.4.4.3 Potential Lipid Biomarkers in the CSF
3.4.5 Blood Biomarkers of AD
3.4.5.1 A&rmbeta
Peptides in Plasma
3.4.5.2 Other Potential Blood Biomarkers
3.4.5.3 Blood Proteins
3.4.6 Blood Lipids
3.4.7 Metabolites
3.4.8 Blood Platelets
3.4.9 Genetic Risk Factors
3.4.10 The Eye as a Window to the Brain
3.4.11 miRNA Tests
3.5 Conclusions
References
Chapter 4 The Link Between Diabetes, Glucose Control, and Alzheimer's Disease and Neurodegenerative Diseases
4.1 Introduction
4.2 The Impact of Type 2 Diabetes on the Brain
4.3 Evidence from Cell Culture, Animal, and Clinical Studies
4.3.1 CNS Insulin Signalling and Disruptions in AD
4.3.2 The Accumulation of A&rmbeta
Is Associated with Impaired Insulin Signalling
4.3.3 Insulin Resistance Promotes the Accumulation of A&rmbeta
4.3.4 Impairments in Insulin Signalling Can Induce Hyperphosphorylation of Tau
4.3.5 Type 2 Diabetes and Neuroinflammation
4.3.6 Oxidative Stress and Mitochondrial Dysfunction in T2D and AD
4.3.7 Targeting Type 2 Diabetes to Slow Down Progression/Prevent Neurodegeneration and Cognitive Decline
4.4 Conclusions
References
Chapter 5 Diet and Nutrition, and their Influence on Alzheimer's Disease and other Neurodegenerative Diseases
5.1 Introduction
5.2 Dietary Patterns
5.3 Key Macronutrients
5.3.1 Dietary Fatty Acids
5.3.2 Cholesterol
5.3.3 Polyunsaturated Fatty Acids
5.3.4 Dietary Carbohydrates
5.4 Key Micronutrients
5.4.1 Water Soluble Vitamins
5.4.1.1 B Vitamins
5.4.2 Fat Soluble Vitamins
5.4.2.1 Vitamin A (Retinol, Retinal, and Retinoic Acid)
5.4.2.2 Vitamin D
5.4.2.3 Vitamin E
5.4.3 Dietary Minerals
5.4.3.1 Selenium
5.4.3.2 Manganese
5.4.3.3 Zinc, Iron, Copper, and Calcium
5.5 Conclusion
References
Chapter 6 Carbohydrate and Protein Metabolism: Influences on Cognition and Alzheimer's Disease
6.1 Carbohydrates
6.1.1 Carbohydrate Digestion
6.1.2 Glucose Ingestion and Use
6.1.3 Glucose and Insulin, Insulin Resistance, and Type 2 Diabetes (Short Summary)
6.1.4 Relative Intake of Carbohydrate and its Impacts on Neurodegenerative Disease Risk
6.1.5 Ketogenic Diets
6.1.6 Glucose and Its Effects on Cognition
6.1.7 Possible Mechanisms Related to Memory Enhancement with Glucose
6.1.7.1 Glucose and the Hippocampus
6.1.7.2 Glucose Availability in Brain Cells
6.1.7.3 Glucose and the Central Cholinergic System
6.1.7.4 ATP-Regulated Potassium (K-ATP) Channels and Brain Control of Glucose Homeostasis
6.1.7.5 Effects of High Fructose Diets
6.1.7.6 Sucrose
6.2 Proteins
6.2.1 Protein Metabolism in General
6.2.2 Links Between Specific Amino Acids and Brain Function
6.2.2.1 Tryptophan
6.2.2.2 Tyrosine
6.2.3 Clinical Studies of Protein Supplementation
6.2.4 Links Between Loss of Protein Function and Neurodegeneration
6.2.5 Clearance Mechanisms Associated with Proteinopathies Involved in Neurodegeneration
6.2.6 Role of Protein Crosslinking and Inflammation in Neurodegeneration and AD
6.3 Conclusion
References
Chapter 7 Fat and Lipid Metabolism and the Involvement of Apolipoprotein E in Alzheimer's Disease
7.1 Introduction
7.2 Alzheimer's Disease
7.3 Cholesterol and Lipid Metabolism
7.3.1 Cholesterol Synthesis and Metabolism
7.3.2 Oxysterols
7.3.2.1 Oxysterols in AD
7.3.3 Pathways of Dietary (Exogenous) Lipid Homeostasis
7.3.4 Pathways of Endogenous Lipid Homeostasis
7.3.5 Peripheral Clearance of Lipoproteins and Reverse Cholesterol Transport
7.3.5.1 Lipoproteins in the CNS
7.4 Apolipoprotein E Alleles and Isoforms
7.4.1 ApoE in the Brain
7.4.2 Apolipoprotein E and Alzheimer's Disease
7.4.2.1 ApoE Binding to A&rmbeta
7.4.2.2 ApoE in the Cellular Clearance of A&rmbeta
7.4.2.3 ApoE and Antioxidant Properties
7.4.2.4 ApoE and Tissue Transglutaminase
7.4.2.5 Apolipoprotein J (Clusterin, CLU)
7.5 LRP-1 in the Brain and Its Role in A&rmbeta
Clearance
7.5.1 LDL, HDL, and AD
7.5.2 Statins, Cholesterol, and AD
7.6 The Role of Lipid Rafts in Neurodegenerative Diseases
7.7 Changes to Glycerophospholipids in Alzheimer's Disease
7.7.1 Omega-3 and Omega-6 Fatty Acids
7.7.1.1 Omega-3 Fatty Acids, Modern Diets, and Health Implications
7.8 Sphingolipids
7.8.1 Ceramides
7.8.2 Sulfatides
7.8.3 Gangliosides
7.9 Conclusions
References
Chapter 8 Inflammation in Alzheimer's Disease, and Prevention with Antioxidants and Phenolic Compounds - What Are the Most Promising Candidates?
8.1 Introduction
8.2 Inflammation and the Immune Response in AD
8.2.1 The Role of Microglia and Astrocytes in Chronic Inflammation in AD
8.3 Oxidative Stress
8.3.1 Advanced Glycation End Products
8.3.2 Involvement of the Complement System in AD
8.3.3 Involvement of Cytokines and Chemokines in Inflammation
8.3.4 Inflammation - Susceptibility to A&rmbeta
Deposition or Aggregation
8.3.5 Inflammation Can Influence A&?Undefined ?&PP Metabolism and A&rmbeta
Clearance Directly
8.4 Current Medications for AD
8.4.1 Current Medications - Acetylcholinesterase Inhibitors and Memantine
8.5 Disease Modification and Treatment Approaches
8.5.1 Non-Steroidal Anti-Inflammatory Drugs (NSAID)
8.6 Some Anti-inflammatory Foods, Supplements, and Newly Developed Drugs for the Treatment of AD
8.6.1 Cinnamon/Cinnamaldehyde
8.6.2 (-)Epigallocatechin-3-Gallate (EGCG) and Other Green Tea Polyphenols
8.6.3 Curcumin
8.6.4 Other Polyphenolic Antioxidants
8.6.5 Omega-3 (n-3) Essential Fatty Acids
8.6.6 Lipoic Acid
8.7 Conclusion
References
Chapter 9 Cognitive Impairments in Alzheimer's Disease and Other Neurodegenerative Diseases
9.1 Introduction
9.2 Dementia due to Alzheimer's Disease
9.2.1 Subjective Cognitive Decline and Mild Cognitive Impairment (MCI)
9.2.2 Memory Impairments in AD
9.2.2.1 Episodic Memory
9.2.2.2 Semantic Memory
9.2.2.3 Prospective Memory (PM)
9.2.3 Attention and Executive Dysfunction in AD
9.2.4 Language
9.2.5 Visuospatial Abilities
9.2.6 Dementia with Lewy Bodies and Parkinson's Disease with Dementia
9.2.7 Vascular Dementia
9.2.8 Frontotemporal Dementia
9.3 Conclusions
References
Chapter 10 Animal Models of Alzheimer's Disease
10.1 Introduction
10.2 Transgenic Mouse Models
10.3 Knock-in AD Mice Models
10.4 Non-Transgenic and Other Mammalian Animal Models
10.5 Drug Development and Translational Issues
10.6 Correlations Between Animal Models of AD and Human AD
10.7 Experimental Design and Reporting
10.8 The Future of Animal Models in AD
References
Chapter 11 The Products of Fermentation and Their Effects on Metabolism, Alzheimer's Disease, and Other Neurodegenerative Diseases: Role of Short-Chain Fatty Acids (SCFA)
11.1 Introduction
11.2 Fermentable Substrates and Short-Chain Fatty Acids
11.2.1 Colonic Microflora and Fermentation
11.2.1.1 Probiotics and Prebiotics
11.2.2 Propionic Acid (PPA)
11.2.3 Acetic Acid
11.2.4 Butyric Acid
11.2.5 Short-Chain Fatty Acids and Free Fatty-Acid Receptor Signalling
11.2.6 Short-Chain Fatty Acids and Energy Intake
11.2.7 Short-Chain Fatty Acids and Energy Expenditure
11.2.8 Regulation of Fatty-Acid Metabolism by SCFA
11.2.9 Effect of Short-Chain Fatty Acids on Glucose Regulation
11.2.10 Regulation of Cholesterol Metabolism by Short-Chain Fatty Acids
11.2.11 Regulation of Inflammation by Short-Chain Fatty Acids
11.2.12 Short-Chain Fatty Acids and Neuroprotection
11.3 Conclusions
References
Chapter 12 Hormonal Expression Associated with Alzheimer's Disease and Neurodegenerative Diseases
12.1 The Hypothalamic-Pituitary-Gonadal (HPG) Axis
12.1.1 Dysregulation of the HPG Axis During Ageing
12.2 Roles for Sex Steroids and Gonadotropins in the Neurodegenerative Process in AD
12.2.1 Sex Steroids Modulate A&rmbeta
Accumulation
12.2.2 Sex Steroids and Oxidative Stress
12.2.3 Sex Steroids and Inflammation
12.2.4 Testosterone and Diabetes
12.2.5 A Role for Gonadotropins in AD Pathogenesis
12.3 Hormone-based Therapies
12.3.1 The Oestrogens
12.3.2 Testosterone Therapy
12.3.3 Selective Oestrogen or Androgen Receptor Modulators (SERM or SARM)
12.3.4 Gonadotropin-Lowering Agents
12.4 Conclusions
References
Chapter 13 The Link Between Exercise and Mediation of Alzheimer's Disease and Neurodegenerative Diseases
13.1 Introduction
13.2 Physical Activity Promotes Health and Well-being
13.3 Neuroplasticity
13.4 The Link Between Physical Activity and Cognition Across the Human Lifespan
13.4.1 Childhood
13.4.2 Adulthood and Midlife
13.4.3 Older Adults
13.5 Physical Activity Reduces the Risk of Dementia and AD
13.6 Mechanisms Underlying the Relationship Between Exercise and Brain Health
13.6.1 Evidence from Molecular and Cellular Research
13.6.2 Neurotrophins
13.6.3 Hormonal Pathways
13.6.4 Cardiovascular and Metabolic Mechanisms
13.6.5 Evidence from Neuroimaging Studies
13.7 The Effect of Genetics on the Relationship Between Exercise and Brain Health
13.8 Future Directions
References
Chapter 14 Current and Prospective Treatments for Alzheimer's Disease (and Other Neurodegenerative Diseases)
14.1 Introduction
14.2 Current and Potential Medical Treatments
14.2.1 Treatments That Influence Neurotransmission
14.2.1.1 Cholinergic System
14.2.1.2 Other Neurotransmitters
14.2.2 Cholesterol-Lowering Medications
14.2.3 Immunotherapy
14.2.3.1 Active Immunotherapy (A&rmbeta
)
14.2.3.2 Active Immunotherapy (tau)
14.2.3.3 Passive Immunotherapy (A&rmbeta
)
14.2.3.4 Passive Immunotherapy (tau)
14.2.4 Targeting the A&rmbeta
-Producing Pathway
14.2.4.1 &rmalpha
-Secretase
14.2.4.2 &rmbeta
-Secretase
14.2.4.3 &rmgamma
-Secretase
14.2.5 Other Compounds Affecting A&rmbeta
14.2.6 Other Compounds Affecting Tau
14.2.7 Inflammatory Targets
14.3 Conclusions
References
Chapter 15 The Role of Genetics in Alzheimer's Disease and Parkinson's Disease
15.1 Introduction
15.2 Genetics of Alzheimer's Disease
15.3 Autosomal Dominant AD (ADAD)
15.3.1 Understanding the Importance of APP and the Presenilins in AD
15.4 Amyloid Precursor Protein (APP)
15.5 Presenilin 1 (PSEN1)
15.6 Presenilin 2 (PSEN2)
15.7 Genetic Contributions to Sporadic Late-Onset AD (LOAD)
15.8 Cholesterol Metabolism
15.8.1 Apolipoprotein E (APOE)
15.8.2 Clusterin (CLU)
15.8.3 ATP-Binding Cassette Transporter A7 (ABCA7)
15.9 Immune Response
15.9.1 Complement Receptor 1 (CR1)
15.9.2 CD33 (Myeloid Cell Surface Antigen CD33
Sialic Acid-Binding Immunoglobulin-Like Lectin 3)
15.9.3 Membrane Spanning 4 Domains, Subfamily A (MS4A)
15.9.4 Triggering Receptor Expressed on Myeloid Cells 2 (TREM2)
15.9.5 Further Genetic Associations Implicating the Immune Response
15.10 Endocytosis
15.10.1 Bridging Integrator 1 (BIN1)
15.10.2 Phosphatidylinositol Binding Clathrin Assembly Lymphoid Myeloid Protein (PICALM)
15.10.3 CD2-Associated Protein (CD2AP)
15.10.4 Further Genetic Associations Implicating Endocytosis
15.10.5 Variants in APP and Genes for APP-Metabolising Proteins
15.10.6 Further Mechanisms Implicated Through Genetic Associations
15.11 Genetics of Parkinson's Disease
15.12 Monogenic forms of PD
15.12.1 Autosomal Dominant Forms
15.12.1.1 PARK 1 (SNCA)
15.12.1.2 PARK 8 (LRRK2)
15.12.1.3 PARK 11 (GIGYF2)
15.12.1.4 PARK 17 (VPS35)
15.12.1.5 PARK 18 (EIF4G1)
15.12.2 Autosomal Recessive Forms
15.12.2.1 PARK 2 (PRKN)
15.12.2.2 PARK 6 (PINK 1)
15.12.2.3 PARK 7 (DJ-1)
15.12.2.4 PARK 9 (ATP13A2)
15.12.2.5 PARK 14 (PLA2G6)
15.12.2.6 PARK 15 (FBXO7)
15.12.3 Genetic Contributions to Late-Onset Sporadic PD (LOPD)
15.12.4 Common Variants in PD Genes
15.12.5 Glucocerebrosidase (GBA)
15.12.6 Immune-Inflammatory Genes
15.12.7 Mitochondrial DNA Variants
15.13 Conclusion
References
Final Thoughts Regarding Alzheimer's Disease, Diet, and Health
List of Abbreviations
Index
EULA

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