Current Thoughts on Dementia

Preface
Acknowledgments
Contents
About the Editors
Part I: Risk Factors for Dementia
	1: ApoE: A Risk Factor for Dementia
		1.1 Introduction
		1.2 Types of Dementia
			1.2.1 Progressive Dementias
				1.2.1.1 Alzheimer´s Disease
				1.2.1.2 Frontotemporal Lobar Degeneration
				1.2.1.3 Alpha-Synucleinopathies
				1.2.1.4 Vascular Dementia
					Mixed Dementia
			1.2.2 Dementias Associated with Other Conditions
				1.2.2.1 Huntington´s Dementia
				1.2.2.2 Traumatic Brain Injury
				1.2.2.3 Creutzfeldt-Jakob Disease
				1.2.2.4 Parkinson´s Disease
		1.3 Risk Factors for Dementia
			1.3.1 Age
			1.3.2 Sex
			1.3.3 Physical Activity
			1.3.4 Smoking
			1.3.5 Comorbidity
			1.3.6 Environmental Factors and Nutrition
			1.3.7 Drugs
			1.3.8 Genetic Effects
		1.4 Structure of ApoE
		1.5 Physiological Functions of ApoE
		1.6 ApoE in Dementia and Associated Diseases
			1.6.1 ApoE and Alzheimer´s Disease
				1.6.1.1 Mechanism of ApoE4 in AD
					Aβ Aggregation and Clearance
					Tau Phosphorylation
					Neuroinflammation
					Synaptic Plasticity
					Lipid Metabolism
			1.6.2 Vascular Dementia and Cerebrovascular Disorders
			1.6.3 Parkinson´s Disease
			1.6.4 Schizophrenia
			1.6.5 Multiple Sclerosis
		1.7 Recent Developments and Future Perspectives
		1.8 Conclusion
		References
	2: Infection-Induced Systemic Inflammation and Dementia
		2.1 Introduction
		2.2 Pathogenesis of Dementia: Prevailing Hypotheses and Their Limitations
			2.2.1 Amyloid Cascade Hypothesis
				2.2.1.1 Limitations of the Amyloid Cascade Hypothesis
			2.2.2 Tau Hypothesis
				2.2.2.1 Limitations of the Tau Hypothesis
			2.2.3 Mitochondrial Cascade Hypothesis
				2.2.3.1 Limitations of the Mitochondrial Cascade Hypothesis
			2.2.4 NMDA Receptor-Mediated Glutamate Excitotoxicity
				2.2.4.1 Limitations of the NMDA Receptor-Mediated Glutamate Excitotoxicity
			2.2.5 Cholinergic Hypothesis
				2.2.5.1 Limitations of the Cholinergic Hypothesis
			2.2.6 Oxidative Stress Hypothesis
				2.2.6.1 Limitations of the Oxidative Stress Hypothesis
		2.3 Infection Theory
			2.3.1 Infection-Induced Systemic Inflammation and Neuroinflammation
				2.3.1.1 Mode of Communication Between the Peripheral Immune System and the CNS
			2.3.2 Infection-Induced Systemic Inflammation and Blood-Brain Barrier Integrity
			2.3.3 Systemic Inflammation and Alzheimer´s Disease Progression
			2.3.4 Role of the Innate and Adaptive Immune System in Dementia Pathology
				2.3.4.1 The Innate Immune System
				2.3.4.2 The Adaptive Immune System
		2.4 Infection and Cognitive Changes in Dementia
		2.5 System Inflammatory Markers and Risk of Dementia
		2.6 Infection-Induced Systemic Inflammatory Mediators as Potential Therapeutic Targets
			2.6.1 Potential Novel and Conventional Pharmacological Agents
				2.6.1.1 NSAIDs
				2.6.1.2 Lipoxin A4
				2.6.1.3 Other Therapeutic Agents
			2.6.2 Phytochemicals
		2.7 Recent Developments and Future Perspectives
		2.8 Conclusion
		References
	3: Role of Impaired Insulin Signaling in the Pathogenesis of Dementia
		3.1 Introduction
		3.2 Brain Insulin
		3.3 Insulin Receptors and Signaling
		3.4 Functions of Insulin in Brain
			3.4.1 Maintain Blood-Brain Barrier Function
			3.4.2 Glucose Homeostasis
			3.4.3 Cognition and Memory
			3.4.4 Inhibit Excitotoxicity and Neuronal Protection
		3.5 Insulin Signaling Impairment Led to Dementia and Related Pathologies
			3.5.1 Insulin Signaling in Dementia Associated with Alzheimer´s Disease
			3.5.2 Insulin Signaling in Dementia Associated with Parkinson´s Disease
			3.5.3 Insulin Signaling in Dementia Associated with Huntington´s Disease
			3.5.4 Insulin Signaling in Dementia Associated with Lewy Body Disease
			3.5.5 Insulin Signaling in Frontotemporal Dementia
		3.6 Neuroinflammation and Impaired Insulin Signaling in Dementia
		3.7 Insulin in the Treatment of Dementia
		3.8 Recent Developments and Future Perspectives
		3.9 Conclusion
		References
	4: Sex Hormones as Risk Factors for Dementia
		4.1 Introduction
		4.2 Sex Hormones
			4.2.1 Aging and Loss of Sex Hormones
			4.2.2 Age-Related Neurodegeneration and Sex Hormones
		4.3 Sex Hormones and the Brain
			4.3.1 Sex Hormones and Synaptic Plasticity
			4.3.2 Sex Hormones and Mitochondrial Function
			4.3.3 Interaction of Sex Hormones and Growth Factors
			4.3.4 Effect of Sex Hormones on Neurosteroidogenesis
			4.3.5 Sex Hormones and Neuroinflammation
			4.3.6 DNA Repair, Sex Hormones, and Brain Aging
			4.3.7 Neuroprotective Effects Exhibited by Sex Hormones
		4.4 Progesterone in Neurodegeneration
		4.5 Recent Developments and Future Perspectives
		4.6 Conclusion
		References
	5: Mitophagy Impairments as Culprit of Alzheimer’s Disease
		5.1 Introduction
		5.2 Alzheimer’s Disease: A Common Form of Dementia
		5.3 Mitochondria and Neuroplasticity in Alzheimer’s Disease
		5.4 Mitophagy in Maintaining Mitochondrial Homeostasis and Alzheimer’s Disease
			5.4.1 Mitophagy Regulated by Parkin-Dependent Pathway
			5.4.2 Mitophagy Regulated by Parkin-Independent Pathway
				5.4.2.1 Ub Ligase-Induced Mitophagy
				5.4.2.2 Receptor-Induced Mitophagy and Lipid-Induced Mitophagy
		5.5 Impaired Mitophagy in Alzheimer’s Diseases
			5.5.1 Aβ and Mitophagy
			5.5.2 Tau and Mitophagy
			5.5.3 Inflammation and Mitophagy
		5.6 Triggering Mitophagy for Therapeutic Interventions in Alzheimer’s Diseases
		5.7 Recent Developments and Future Perspectives
		5.8 Conclusion
		References
	6: Parkinson´s Disease: Neurochemistry and Pharmacological Treatment
		6.1 Introduction
		6.2 Pathogenesis of Parkinson´s Disease
			6.2.1 α-Synuclein and Formation of Lewy Bodies
				6.2.1.1 Association Between α-Synuclein and Autophagy-Lysosome Pathway
				6.2.1.2 Synucleinopathy and Endoplasmic Reticulum Stress Response
			6.2.2 Disturbances in Mitochondrial Functions
			6.2.3 Iron Accumulation and Oxidative Stress
			6.2.4 Inflammation and Gliosis
			6.2.5 Neurotransmitters and Neuropeptides Associated with Parkinson´s Disease
				6.2.5.1 Dopamine
				6.2.5.2 Acetylcholine
				6.2.5.3 Serotonin
				6.2.5.4 Role of GABA/Ca2+ System
				6.2.5.5 Glutamate
				6.2.5.6 Cholecystokinin
				6.2.5.7 Dynorphin
				6.2.5.8 Neurotensin
				6.2.5.9 Substance P
		6.3 Treatment Approach for Parkinson´s Disease
		6.4 Recent Advancement and Future Perspectives
			6.4.1 Surgical Treatments
			6.4.2 Neural Transplantation Therapy
			6.4.3 Gene Therapy
			6.4.4 Experimental Research
		6.5 Conclusion
		References
	7: Emerging Roles of TREM2 in Neurodegenerative Diseases
		7.1 Introduction
		7.2 Expression Pattern and Structure of TREM2
		7.3 Regulation of TREM2 Signaling Pathways
		7.4 TREM2-Dependent Cellular Responses
		7.5 Neurodegenerative Disease-Associated Mutations in TREM2
		7.6 TREM2-Mediated Demyelination and Remyelination
		7.7 Role of TREM2 in Neurodegenerative Diseases
			7.7.1 Frontotemporal Dementia
			7.7.2 Alzheimer´s Disease
			7.7.3 Parkinson´s Disease
			7.7.4 Polycystic Lipomembranous Osteodysplasia with Sclerosing Leukoencephalopathy
			7.7.5 Amyotrophic Lateral Sclerosis
			7.7.6 Other Neurodegenerative Diseases
		7.8 Therapeutic Interventions to Tackle TREM2
		7.9 Recent Developments and Future Perspectives
		7.10 Conclusion
		References
	8: Molecular Mechanisms Underlying the Role of HSPB8 in Neurodegeneration
		8.1 Introduction
		8.2 Protein Quality Control System in Neurodegeneration
		8.3 Distribution of HSPB8
			8.3.1 Structure of HSPB8
		8.4 sHSP in Neurodegenerative Disorders
			8.4.1 Role of HSPB8 in Motor Neuron Diseases
			8.4.2 Role of HSPB8 in Amyotrophic Lateral Sclerosis and Muscular Atrophy
			8.4.3 Role of HSPB8 in Alzheimer´s Disease
			8.4.4 Role of HSPB8 in Parkinson´s Disease
			8.4.5 Role of HSPB8 in Huntington´s Disease
			8.4.6 Role of HSPB8-BAG3 Induction in Motor Neuron Diseases
		8.5 Recent Development and Future Perspectives
		8.6 Conclusion
		References
	9: Molecular Insights into the Role of ER Stress in Neurodegenerative Diseases
		9.1 Introduction
		9.2 ER Stress-Induced Neuronal Cell Death Mechanisms
		9.3 Role of Endoplasmic Reticulum Stress in Neurodegenerative Diseases
			9.3.1 Alzheimer´s Disease
			9.3.2 Parkinson´s Disease
			9.3.3 Amyotrophic Lateral Sclerosis
			9.3.4 Huntington´s Disease
			9.3.5 Prion-Related Disorders
		9.4 ER Stress and Acute Neurodegeneration
		9.5 Recent Developments and Future Perspectives
		9.6 Conclusion
		References
	10: Role of Hypertension and Hyperlipidemia in the Pathogenesis of Dementia
		10.1 Introduction
		10.2 Hypertension in the Emergence of Dementia
		10.3 Hyperlipidemia in the Emergence of Dementia
		10.4 Relationship Between Aging, Hypertension, Hyperlipidemia, and Dementia
		10.5 Drugs Used in the Treatment of Dementia
		10.6 Recent Developments and Future Perspectives
		10.7 Conclusion
		References
	11: Behavioral Abnormalities of Gut Microbiota and Progression of Dementia
		11.1 Introduction
		11.2 Formation of the Normal Gut Microbiota
			11.2.1 Gut-Brain Axis
			11.2.2 Impact of Gut Microbiota on Behavioral and Functional Aspects of Brain
			11.2.3 Present Understanding Related to Gut Microbiota
		11.3 Dementia
			11.3.1 Factors Associated with Dementia
				11.3.1.1 Diabetes, Hypertension, and Obesity
				11.3.1.2 Smoking
				11.3.1.3 Depression
		11.4 Behavioral Abnormalities and Progression of Dementia
			11.4.1 Specific Risk Factors and Mechanisms
			11.4.2 Education or Qualification of Individuals
			11.4.3 Hearing
			11.4.4 Exercise and Physical Activity
		11.5 Behavioral and Psychological Symptoms of Dementia
		11.6 Relationship Between Dementia and Gut Microbiota
		11.7 Factors Impacting the Normal Gut Microbiota
			11.7.1 Child´s Age
			11.7.2 Diet
			11.7.3 Antibiotics
		11.8 Recent Developments and Future Perspectives
		11.9 Conclusion
		References
	12: Gut-Brain Axis in Alzheimer´s Disease: Interplay Between Cholecystokinin, Dysbiosis, and Brain-Derived Neurotrophic Factor
		12.1 Introduction
		12.2 Cholecystokinin Physiology
		12.3 Mechanism of Cholecystokinin Signaling from the Gut to the Brain
		12.4 The Link Between Cholecystokinin and Alzheimer´s Disease
		12.5 The Link Between Cholecystokinin and Alzheimer´s Disease Risk Factors
			12.5.1 A Promising Connection Between Brain-Derived Neurotrophic Factor and Alzheimer´s Disease
			12.5.2 CCK Mediates Brain-Derived Neurotrophic Factor Release
			12.5.3 Obesity as a Risk Factor for Alzheimer´s Disease
			12.5.4 Cholecystokinin Correlations with Hyperphagia and Obesity
			12.5.5 Crosstalk of Gut Microbiota and Alzheimer´s Disease and Cholecystokinin
		12.6 Linkage of Cholecystokinin and Ketone Bodies in Alzheimer´s Disease
		12.7 Changes in Cholecystokinin System in Other Dementia Subtypes
		12.8 Recent Developments and Future Perspectives
		12.9 Conclusion
		References
Part II: Therapeutic Interventions for Dementia
	13: Cholesterol and Dementia: A Possible Therapeutic Approach
		13.1 Introduction
		13.2 Dementia and Its Relationship with Cholesterol
		13.3 Cholesterol Metabolism and Homeostasis in the Brain
		13.4 Cholesterol Levels and Dementia
			13.4.1 Role of Cholesterol in Amyloid Plaques
			13.4.2 Role of Cholesterol in Tau Protein
		13.5 Cholesterol Metabolism as a Therapeutic Strategy for Dementia
			13.5.1 ACAT1/SOAT1 as a Therapeutic Target
				13.5.1.1 ACAT1 Inhibitors
			13.5.2 Statin Therapy as a Possible Therapeutic Strategy
		13.6 Recent Developments and Future Perspectives
		13.7 Conclusion
		References
	14: Therapeutic Potential of PPARs in Alzheimer´s Disease
		14.1 Introduction
		14.2 Historical Outlook of the Peroxisomes
		14.3 Molecular Structure of PPARs
			14.3.1 N-Terminal (A/B Domain)
			14.3.2 DNA Binding Domain (C-domain, DBD)
			14.3.3 Hinge Region
			14.3.4 Carboxyl Terminal (E/F Domain)
			14.3.5 Ligand Binding Domain
		14.4 Tissue Distribution and Expression of PPARS and Their Target Genes
			14.4.1 PPARα
			14.4.2 PPARβ/δ
			14.4.3 PPARγ
		14.5 PPAR During Development
		14.6 Isoforms of PPARs and Their Ligands
			14.6.1 PPARα
			14.6.2 PPARγ
			14.6.3 PPARβ/δ
			14.6.4 Ligand Binding of PPARs
			14.6.5 PPAR Signaling
		14.7 Pathophysiology of Neuroinflammation in Alzheimer´s Disease
			14.7.1 Basis for the Use of PPAR Agonists in Alzheimer´s Disease
		14.8 PPARγ, Genetics, and Dyslipidemia in Alzheimer´s Disease
		14.9 PPARγ and Neuroinflammation in Alzheimer´s Disease
		14.10 PPARγ and Energy Metabolism in the Mitochondria of Alzheimer´s Disease
		14.11 PPARγ, Insulin Signaling, and Metabolism in Alzheimer´s Disease
		14.12 PPARγ and Canonical Wnt/β-Catenin Signaling in Alzheimer´s Disease
		14.13 PPARγ and Neurofibrillary Tangles
		14.14 Recent Developments and Future Perspectives
		14.15 Conclusion
		References
	15: Exploring the Role of Statins in Reversing the Cognitive and Neurovascular Dysfunctions in Dementia
		15.1 Introduction
		15.2 Synergistic Interaction of Vascular and Neurodegenerative Pathologies
		15.3 Neurovascular Dysregulation Initiated Cognitive Impairment
		15.4 Effect of Pharmacodynamic Parameters of Statins in Central Nervous System
		15.5 Statin and Its Influence in Modulating Neurodegenerative Pathologies
		15.6 Statins and its Their Related Mechanisms in Neurodegenerative Disorders
		15.7 Role of Statins in Reducing Vascular Dementia
		15.8 Role of Statins in Reducing Alzheimer´s Disease Pathology
		15.9 Role of Statins in Reducing Parkinson´s Disease Pathology
		15.10 Role of Statins in Reducing Huntington´s Disease Pathology
		15.11 Regulation of tau and Abeta by Statins
		15.12 Neurovascular Unit Dysregulation Initiated Cognitive Impairment
		15.13 Adversities with the Use of Statins
		15.14 Status of Statin-Based Clinical Studies
		15.15 Recent Developments and Future Perspectives
		15.16 Conclusion
		References
	16: Role of Immunotherapy in Ameliorating Proteopathic Dementia
		16.1 Introduction
		16.2 Global Scenario of Dementia and Its Types
		16.3 Mechanisms of Protein Toxicity in Neurodegenerative Dementias
		16.4 Mechanisms of Protein Toxicity in Dementia of Alzheimer´s Type
			16.4.1 Amyloid Cascade Hypothesis
			16.4.2 Mitochondrial Cascade Hypothesis
			16.4.3 Lipid Peroxidation Malfunctioning
		16.5 Genetic Mechanisms Involved in Dementia
		16.6 RNS-ROS Generated Stress in Dementia
		16.7 Neuroinflammatory Complex Generated Stress in Dementia
		16.8 Therapeutic Approaches for Dementia
			16.8.1 Pharmacological Interventions
			16.8.2 Non-Pharmacological Intervention
		16.9 Targeting Protein Accumulation by Immunotherapy for Dementia
		16.10 Immunotherapeutic Approaches for Dementia
		16.11 Antibody Engineering for Optimized Immunotherapy against Dementia
		16.12 Recent Developments and Future Perspectives
		16.13 Conclusion
		References
	17: Hypoxic-Hyperoxic Training in Dementia
		17.1 Introduction
		17.2 Epidemiology, Clinical Spectrum, and Burden of Dementia
		17.3 Pathophysiology of Dementia with a Focus on Abeta Plaques
		17.4 The Role of Hypoxia in Neurodegeneration and Dementia
		17.5 Hypoxic-Hyperoxic Training on Cognitive Performance
		17.6 Evidence from Preclinical Studies for Hypoxia-Hyperoxia Treatment
		17.7 Evidence from Clinical Studies for Hypoxia-Hyperoxia Treatment
		17.8 Hypoxia-Hyperoxia Treatment: Assessment of the Evidence
		17.9 The Bibliometric Footprint of Hypoxic-Hyperoxic Training Research
		17.10 Hypoxia-Hyperoxia Treatment in the Context of Contemporary Healthcare
		17.11 Recent Developments and Future Perspectives
		17.12 Conclusion
		References
	18: Music Therapy in Dementia
		18.1 Introduction
		18.2 Risk Factors of Dementia
		18.3 Stages of Dementia
			18.3.1 Mild Cognitive Impairment
			18.3.2 Early Stage Dementia
			18.3.3 Middle Stage Dementia
			18.3.4 Late Stage Dementia
		18.4 Types of Dementia
			18.4.1 Alzheimer´s Disease
			18.4.2 Vascular Dementia
			18.4.3 Dementia with Lewy Bodies
			18.4.4 Fronto-Temporal Dementia
			18.4.5 Huntington´s and Parkinson´s Diseases
			18.4.6 Corticobasal Degeneration
			18.4.7 Creutzfeldt-Jacob Disease
			18.4.8 Mixed Dementia
		18.5 Music Therapy: A Healer in Disguise
		18.6 Mechanisms of Action of Music Therapy
			18.6.1 Regeneration Mechanism of the Neurons
			18.6.2 Involvement of Neuroendocrine Pathway
			18.6.3 Neuropsychiatric Mechanism
			18.6.4 Neuroplasticity Mechanism
		18.7 Case Studies Associated with Music Therapy and Its Effect on Brain Function and Dementia
			18.7.1 Effect of Music Therapy on Brain Function
				18.7.1.1 Effect of Music Therapy on Preterm Babies Mental and Overall Development
				18.7.1.2 Effect of Music Therapy on Brain Function
			18.7.2 Case Studies Based on the Detailed Response of Dementia Patients
				18.7.2.1 Effects of Music on Agitated -Type Behavior
				18.7.2.2 Indian Classical Music and Dementia
			18.7.3 Case Studies Including Carer/Nurse Training
				18.7.3.1 Carer Training (Ridder, Denmark)
				18.7.3.2 Training Social Workers and Caregivers in the Family (Wosch, Germany)
				18.7.3.3 Polyphonic Partnerships (Stige, Norway)
			18.7.4 Case Studies Based on Song-Writing
				18.7.4.1 Therapeutic Songwriting for the Family Caregivers (Baker, Australia)
				18.7.4.2 Songwriting by the Patient
		18.8 Recent Developments and Future Perspectives
			18.8.1 Implications of Music Therapy for Clinical Practice
				18.8.1.1 Musical Intervention in Improving the Quality of Life
				18.8.1.2 Musical Intervention in the Depressive State
				18.8.1.3 Impact of Music on Memory
		18.9 Conclusion
		References
	19: Beneficial Effects of Citrus Flavonoids Against Aβ Pathology in Alzheimer´s Disease
		19.1 Introduction
		19.2 Mechanism of Aβ Production and Deposition in Alzheimer´s Disease
		19.3 Role of Aβ in the Pathogenesis of Alzheimer´s Disease
		19.4 Major Risk Factors for Alzheimer´s Disease
		19.5 Flavonoids for the Treatment of Neurodegenerative Events and Alzheimer´s Disease
			19.5.1 Inhibition of Aβ by Hesperidin, Neohesperidin, and Hesperitin
			19.5.2 Inhibition of Aβ by Naringin and Naringenin
			19.5.3 Inhibition of Aβ by Quercetin, Myricetin, and Apigenin
		19.6 Recent Developments and Future Perspectives
		19.7 Conclusion
		References
	20: Therapeutic Potential of Phytochemicals: Lessons Learned from Streptozotocin-Induced Sporadic Alzheimer´s Disease
		20.1 Introduction
		20.2 Function of Brain Insulin and its Signaling Pathways
		20.3 Relationship between Sporadic Alzheimer´s Disease and Impaired Brain Glucose/Energy Metabolism
		20.4 Role of Oxidative Stress in the Development of Sporadic Alzheimer´s Disease
		20.5 Streptozotocin-Induced Experimental Model of Sporadic Alzheimer´s Disease for the Evaluation of Therapeutic Agents
		20.6 Phytochemicals for the Treatment of Streptozotocin-Induced Sporadic Alzheimer´s Disease
		20.7 Recent Developments and Future Perspectives
		20.8 Conclusion
		References
	21: Concept of Amnesia and Dementia in the Unani System of Medicine
		21.1 Introduction
		21.2 Prevalence of Amnesia and Dementia
		21.3 The Basic Concept of Unani System of Medicine
			21.3.1 Amnesia and Dementia
			21.3.2 Etiology of Amnesia and Dementia
			21.3.3 Types of Amnesia and Dementia
			21.3.4 Risk Factors for the Development of Amnesia and Dementia
			21.3.5 Pathogenesis of amnesia and Dementia
			21.3.6 Diagnosis of Amnesia and Dementia
		21.4 Management of Amnesia and Dementia
			21.4.1 Principles of Treatment (Usul-i`Ilāj)
			21.4.2 Life Style Changes
			21.4.3 Dietary Recommendations
			21.4.4 Dietary Restrictions
			21.4.5 Regimenal Therapy (Ilaj Bit Tadbīr)
			21.4.6 Pharmacotherapy (`Ilāj bi´l-Dawā´)
				21.4.6.1 Mufradat (Single Drug) for the Management of Amnesia and Dementia
				21.4.6.2 Pharmacopeial Formulations (Qarābādīni Murakkab) for the Management of Amnesia and Dementia
				21.4.6.3 Compound Formulations (Murakkab) Prepared as per the Need for the Management of Amnesia and Dementia
		21.5 Conclusion
		References
	22: Nanotechnological Applications in the Diagnosis and Treatment of Alzheimer´s Dementia
		22.1 Introduction
		22.2 Nanotechnology in Alzheimer´s Disease
		22.3 Nanotechnology-Based Drug Delivery Systems for Alzheimer´s Disease
			22.3.1 Polymeric Nanoparticles
			22.3.2 Solid Lipid Carriers
			22.3.3 Liposomes
			22.3.4 Surfactant-Based Systems
				22.3.4.1 Microemulsions
				22.3.4.2 Nanoemulsions
				22.3.4.3 Liquid Crystals
			22.3.5 Carbon Nanomaterials
				22.3.5.1 Carbon Nanotube
				22.3.5.2 Fullerene
			22.3.6 Inorganic Nanoparticles
			22.3.7 Magnetic Nanoparticles
			22.3.8 Gold Nanoparticles
			22.3.9 Dendrimers
			22.3.10 Cubosomes
			22.3.11 Antibody-Tethered Nanoparticles
		22.4 Diagnostic Approaches in Alzheimer´s Disease
			22.4.1 Nanodiagnostic Approaches for Alzheimer´s Disease
		22.5 Nanotherapy for Alzheimer´s Disease
			22.5.1 Synthetic Approaches
				22.5.1.1 Rivastigmine
				22.5.1.2 Donepezil
				22.5.1.3 Tacrine
				22.5.1.4 Memantine
			22.5.2 Herbal Approaches
				22.5.2.1 Curcumin
				22.5.2.2 Chlorogenic Acid
				22.5.2.3 Asiatic Acid
				22.5.2.4 Piperine
				22.5.2.5 Resveratrol
				22.5.2.6 Rosmarinic Acid
				22.5.2.7 Astaxanthin
				22.5.2.8 Epigallocatechin-3-Gallate
				22.5.2.9 Huperzine A
				22.5.2.10 Hesperidin
				22.5.2.11 Quercetin
				22.5.2.12 Galantamine
				22.5.2.13 Berberine
		22.6 Recent Developments and Future Perspectives
		22.7 Conclusion
		References
Index