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Diabetes and Neurodegeneration.
- Format:
- Book
- Author/Creator:
- Bagchi, Debasis.
- Language:
- English
- Subjects (All):
- Diabetes.
- Cognition disorders.
- Physical Description:
- 1 online resource (1321 pages)
- Edition:
- 1st ed.
- Place of Publication:
- Chantilly : Elsevier Science & Technology, 2025.
- Summary:
- Diabetes and Neurodegeneration unlocks the complex interplay between diabetes and Neurodegeneration, reviewing the relationship between these two prevalent health challenges.This book begins with a simple guide to understanding high blood sugar, tracing the historical milestones of hyperglycemia, and unveiling the primary factors that contribute.
- Contents:
- Front Cover
- Diabetes and Neurodegeneration
- Copyright Page
- Dedication
- Contents
- List of contributors
- Preface
- Hyperglycemia to neurodegeneration: clinical correlations and molecular cross talks
- I. Introduction: pathogenesis of diabetes and dementia
- 1 Why and when does one have high blood sugar?
- 1.1 Introduction
- 1.2 Blood sugar regulation: the physiological mechanisms
- 1.2.1 Role of hormones in glucose homeostasis
- 1.2.1.1 Insulin: the blood sugar regulator
- 1.2.1.2 Glucagon: the counterregulatory hormone
- 1.2.1.3 Counterregulatory hormones: a complex network
- 1.2.2 Role of organ
- 1.2.2.1 Pancreas: the master regulator
- 1.2.2.2 Liver: the glucose reservoir
- 1.2.2.3 Muscles: the glucose sink and source
- 1.2.2.4 Interactions between organs
- 1.3 Causes of high blood sugar
- 1.3.1 Endogenous factors
- 1.3.1.1 Insulin resistance and insufficiency
- 1.3.1.2 Hormonal dysregulation
- 1.3.2 Exogenous factors
- 1.3.2.1 Diet: high glycemic index foods
- 1.3.2.2 Sedentary lifestyle
- 1.3.2.3 Stress-induced hyperglycemia
- 1.4 Prevention and control
- 1.4.1 Lifestyle adjustments
- 1.4.1.1 Dietary modifications
- 1.4.1.2 Regular physical activity
- 1.4.1.3 Weight management
- 1.4.1.4 Reducing stress
- 1.4.1.5 Adequate sleep
- 1.5 Conclusion
- References
- 2 The history of hyperglycemia: key milestones in the inception of the disease in human health
- 2.1 Introduction
- 2.2 Early narratives
- 2.3 Modern Europe steps in
- 2.4 Search for a treatment: the preinsulin era
- 2.5 Foundation stones for insulin discovery
- 2.6 Initial attempts at insulin isolation
- 2.7 The name is insulin
- 2.8 Diabetes gets its first drug
- 2.9 More on insulin
- 2.10 Nobel prizes
- 2.11 Other antihyperglycaemic agents
- 2.12 Sodium glucose co-transporter 2 inhibitors
- 2.13 Conclusion.
- 3 Walking the sugar-laden path: how diabetes got rooted in human civilization
- 3.1 Introduction
- 3.2 Brief history
- 3.2.1 The role of the pancreas and its association with hyperglycemia
- 3.3 Development of assorted diagnostic procedures
- 3.3.1 Urinary dry-reagent testing
- 3.3.2 Blood glucose dry reagent test strips
- 3.3.3 Biosensor blood glucose meters
- 3.3.4 Advancements in blood glucose monitoring systems
- 3.4 Categorization of diabetes
- 3.4.1 Type 1 diabetes (absolute deficiency of insulin due to β-cell damage)
- 3.4.1.1 Immune-mediated diabetes
- 3.4.1.2 Idiopathic diabetes
- 3.4.2 Type 2 diabetes (varies from insulin secretory failure caused by insulin resistance to insulin resistance alongside relative insulin insufficiency)
- 3.4.3 Secondary forms of diabetes
- 3.4.3.1 Monogenic diabetes
- 3.4.4 Notable genetic diabetes forms
- 3.5 Genetic impairments in insulin action
- 3.5.1 Chemicals or drugs induced diabetes
- 3.5.2 Exocrine pancreatic disorders
- 3.5.3 Endocrinopathies
- 3.5.4 Nonclassical immune-mediated diabetes
- 3.5.5 Other genetic disorders linked with diabetes
- 3.6 Gestational diabetes mellitus
- 3.7 Latest therapeutic approaches and integrated management practices
- 3.8 Conclusion
- 4 Neurodegeneration: how to identify the primary symptoms of cognitive impairment
- 4.1 Introduction
- 4.2 Relationship between mild cognitive impairment and dementia
- 4.3 Early detection of cognitive impairment
- 4.4 Common early symptoms of cognitive impairment
- 4.5 Alzheimer's disease
- 4.6 Frontotemporal dementia
- 4.7 Lewy body dementia
- 4.8 Neuropsychiatric symptoms in dementia
- 4.9 Role of biomarkers in early diagnosis of cognitive impairment
- 4.10 Role of neuropsychological testing
- 4.11 Role of primary caregivers in early diagnosis
- 4.12 Conclusion
- References.
- 5 Risk of dementia in diabetes mellitus: a mechanistic endeavor
- 5.1 Introduction
- 5.1.1 Diabetes mellitus
- 5.1.2 Glycated hemoglobin and formation of advanced glycation end products
- 5.2 Different types of dementia
- 5.2.1 Alzheimer's disease
- 5.2.2 Other dementing disorders
- 5.2.2.1 Progressive supranuclear palsy
- 5.2.2.2 Pick's disease
- 5.2.2.3 Corticobasal degeneration
- 5.2.2.4 Frontotemporal dementia with parkinsonism linked to chromosome 17
- 5.2.2.5 Lewy bodies dementia
- 5.2.2.6 Vascular dementia
- 5.2.3 Relationship between diabetes mellitus and dementia
- 5.2.4 Diabetes management and its impact on dementia
- 5.3 Concluding remarks
- Funding
- Conflict of interest
- Acknowledgment
- 6 Direct consequences of diabetes on the nervous system: structural and molecular pathological changes
- 6.1 Introduction
- 6.2 Diabetic neuropathy
- 6.2.1 Classification
- 6.3 Diabetic neuropathy pathology
- 6.3.1 Symmetrical sensorimotor neuropathy
- 6.3.1.1 Sensory nerves
- 6.3.1.2 Motor nerves
- 6.3.2 Asymmetrical diabetic neuropathies
- 6.3.3 Diabetic autonomic neuropathy
- 6.3.4 DPN lower extremity pathology
- 6.4 Diabetic neuropathy in the spinal cord
- 6.5 Diabetic mononeuropathies
- 6.6 Diabetic radiculopathies
- 6.7 Diabetic retinopathy
- 6.7.1 Neurovascular unit alterations
- 6.7.2 Neuronal alterations
- 6.7.3 Retinal glial alterations
- 6.7.4 Inflammation and oxidative stress
- 6.8 Diabetic autonomic neuropathy
- 6.8.1 Diabetic cardiac autonomic neuropathy
- 6.8.2 Gastrointestinal autonomic neuropathy
- 6.8.3 Urogenic autonomic neuropathy
- 6.8.4 Sudomotor dysfunction
- 6.9 Molecular mechanisms of diabetic neuropathy
- 6.9.1 Insulin signaling and insulin resistance
- 6.9.2 Oxidative stress
- 6.9.3 Mitochondrial energy imbalance and dysfunction.
- 6.9.4 Polyol pathway and altered phosphoinositide metabolism
- 6.9.5 Glycation and advanced glycosylation end products
- 6.9.6 Hexosamine pathway
- 6.9.7 Protein kinase C pathway
- 6.9.8 PARP pathway
- 6.9.9 Neurotrophic substances
- 6.9.10 Nerve barrier disruption
- 6.9.11 Microvascular impairment
- 6.9.12 Inflammation
- 6.9.12.1 Phosphatidylinositol 3-kinase/Akt pathway
- 6.9.12.2 Nuclear factor Kβ pathway
- 6.9.12.3 Mitogen-activated protein kinase pathway
- 6.9.12.4 Tumor necrosis factor-alpha
- 6.9.12.5 Immune cells in diabetic neuropathy
- 6.9.13 Gene expression and regulation
- 6.10 Cognitive disability
- 6.10.1 Alterations in glucose metabolism
- 6.10.2 Brain structural alterations
- 6.11 Alzheimer's disease
- 6.11.1 Alterations in glucose metabolism
- 6.11.2 Insulin signaling alterations
- 6.11.3 Protein pathology
- 6.11.3.1 Aβ peptide
- 6.11.3.2 Tau
- 6.11.3.3 Apolipoprotein A
- 6.11.4 Neuroinflammation
- 6.12 Parkinson's disease
- 6.13 Dementia
- 6.14 Diabetic encephalopathy
- 6.15 Molecular mechanisms linking metabolic disease with cognitive decline
- 6.15.1 Central insulin signaling and resistance
- 6.15.1.1 Glucose tolerance
- 6.15.1.2 Insulin imbalance
- 6.15.1.3 Insulin receptors
- 6.15.2 Blood-brain barrier alterations and cerebral microvascular dysfunction
- 6.15.2.1 Blood- brain barrier breakdown
- 6.15.3 Proteotoxicity
- 6.15.3.1 β-Amyloid metabolism
- 6.15.3.2 Tau protein
- 6.15.3.3 Amylin accumulation
- 6.15.4 Oxidative stress
- 6.15.5 Nuclear factor erythroid 2-related factor 2
- 6.15.6 Mitochondrial dysfunction
- 6.15.7 Neuroinflammation
- 6.15.7.1 Microglial activation
- 6.15.7.2 Astrocyte reactivity
- 6.15.8 Neurotransmitters and neurotrophic substances
- 6.15.8.1 Dopamine
- 6.15.8.2 Serotonin
- 6.15.8.3 Gamma-aminobutyric acid/Glutamate alterations.
- 6.15.8.4 Brain-derived neurotrophic factor
- 6.15.8.5 Acetylcholine, norepinephrine, and epinephrine
- 6.16 Conclusion
- Abbreviations
- II. Discovering the bridge between diabetes and dementia
- 7 Link between hyperglycemia and onset of neurodegeneration: Early clinical evidence
- 7.1 Introduction
- 7.2 Hyperglycemia: definitions and clinical significance
- 7.3 Clinical significance
- 7.4 Neurodegeneration: an overview
- 7.4.1 Major neurodegenerative diseases
- 7.4.1.1 Alzheimer's disease
- 7.4.1.2 Parkinson's disease
- 7.4.1.3 Amyotrophic lateral sclerosis
- 7.4.1.4 Huntington's disease
- 7.4.1.5 Multiple sclerosis
- 7.4.2 Pathophysiological mechanisms (Verdile et al., 2015)
- 7.4.3 Epidemiological evidence linking hyperglycemia to neurodegeneration
- 7.4.4 Alzheimer's disease
- 7.4.4.1 Increased risk
- 7.4.4.2 Accelerated cognitive decline
- 7.4.5 Parkinson's disease
- 7.4.5.1 Higher incidence
- 7.4.5.2 Disease progression
- 7.4.5.3 Potential mechanisms
- 7.4.6 Amyotrophic lateral sclerosis
- 7.4.6.1 Inconclusive evidence
- 7.4.6.2 Future research needs
- 7.4.7 Other neurodegenerative disorders
- 7.4.7.1 Huntington's disease and multiple sclerosis
- 7.4.8 Influence of duration and glycemic control
- 7.4.8.1 Duration of diabetes
- 7.4.8.2 Glycemic control
- 7.4.9 Demographic and genetic factors
- 7.4.9.1 Age, gender, and ethnicity
- 7.4.9.2 Genetic predispositions
- 7.4.10 Clinical studies and observations
- 7.4.11 Brain imaging studies
- 7.4.11.1 Structural magnetic resonance imaging
- 7.4.11.2 Diffusion tensor imaging
- 7.4.11.3 Functional magnetic resonance imaging
- 7.4.11.4 Positron emission tomography
- 7.4.12 Biomarkers of neurodegeneration in hyperglycemia
- 7.4.12.1 Amyloid-beta and tau proteins
- 7.4.12.2 Inflammatory cytokines
- 7.4.12.3 Oxidative stress markers.
- 7.4.12.4 Neurofilament light chain.
- Notes:
- Description based on publisher supplied metadata and other sources.
- Part of the metadata in this record was created by AI, based on the text of the resource.
- ISBN:
- 0-443-33356-4
- 9780443333569
- OCLC:
- 1558597956
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