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Advances in Alzheimer's disease (Series) ;.
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Table of Contents
- Title Page
- Preface
- Introduction
- Contents
- SECTION 1: A neglected side of Alzheimer's research
- Microbes and Alzheimer's Disease
- SECTION 2: Inflammation and Alzheimer's disease
- Inflammation, Anti-inflammatory Agents, and Alzheimer's Disease: The Last 22 Years
- Inflammasome Involvement in Alzheimer's Disease
- Inflammatory Aspects of Alzheimer Disease and Other Neurodegenerative Disorders
- SECTION 3: Bacterial infection and Alzheimer's disease
- Chlamydia Pneumoniae as an Etiologic Agent for Late-Onset Alzheimer's Disease
- Chronic Inflammation and Amyloidogenesis in Alzheimer's Disease - Role of Spirochetes
- Borrelia Burgdorferi Persists in the Brain in Chronic Lyme Neuroborreliosis and may be Associated with Alzheimer Disease
- Statistical Evidence for a Lack of Correlation between the Incidence of Lyme Disease and Deaths Due to Alzheimer's Disease
- Alzheimer's Disease: Assessing the Role of Spirochetes, Biofilms, the Immune System, and Amyloid-Beta with Regard to Potential Treatment and Prevention
- Bacterial Amyloid and DNA are Important Constituents of Senile Plaques: Further Evidence of the Spirochetal and Biofilm Nature of Senile Plaques
- Determining the Presence of Periodontopathic Virulence Factors in Short-Term Postmortem Alzheimer's Disease Brain Tissue
- Active Invasion of Porphyromonas gingivalis and Infection-Induced Complement Activation in ApoE-/- Mice Brains
- Bacterial Burden in Disease, Aging and Alzheimer's Disease
- Bacterial Infection Increases the Risk of Alzheimer's Disease: An Evidence-Based Assessment
- SECTION 4: Periodontal disorders and Alzheimer's disease
- Alzheimer's Disease and Peripheral Infections: The Possible Contribution from Periodontal Infections, Model and Hypothesis
- Putative Association of Periodontitis with Alzheimer's Disease
- SECTION 5: Viral infections and Alzheimer's disease
- Herpes and Alzheimer's Disease: Subversion in the Central Nervous System and How It Might Be Halted
- Herpes Simplex Virus Type 1 Neuronal Infection Elicits Cellular and Molecular Mechanisms of Neuroinflammation and Neurodegeneration in in vitro and in vivo Mice Models
- Anti-Viral Properties of Amyloid-Beta Peptides
- Herpes Simplex Virus Type 1 and Other Pathogens are Key Causative Factors in Sporadic Alzheimer's Disease
- SECTION 6: Fungal infection and Alzheimer's disease
- Alzheimer's Disease and Fungal Infection
- SECTION 7: Bacterial amyloid, iron, homocysteine, ApoE, and Alzheimer's disease
- Amyloid: Friend and Foe
- A Bacterial Component to Alzheimer's-Type Dementia Seen via a Systems Biology Approach that Links Iron Dysregulation and Inflammagen Shedding to Disease
- Iron Withholding: A Defense Against Disease
- Homocysteine, Infections, Polyamines, Oxidative Metabolism, and the Pathogenesis of Dementia and Atherosclerosis
- Apolipoprotein E Related Co-Morbidities and Alzheimer's Disease
- SECTION 8: Gene signature and environmental factors in Alzheimer's disease
- Gene Signature in Alzheimer's Disease and Environmental Factors: The Virus Chronicle
- SECTION 9: Bacterial lipopolysaccharide and pathogen free conditions related to Alzheimer's disease
- Bacterial Lipopolysaccharide (LPS) and Alzheimer's Disease
- Pathogen Free Conditions Slow the Onset of Neurodegeneration in a Mouse Model of Nerve Growth Factor Deprivation
- Subject Index
- Author Index
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