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Alzheimer Disease ll: Pathophysiology

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Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...

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The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...

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Related Experiment Video

Updated: Jul 17, 2026

Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

Published on: December 26, 2016

Inflammatory processes in Alzheimer's disease.

Michael T Heneka¹, M Kerry O'Banion

¹Department of Neurology, Molecular Neurology Unit, University of Münster, Mendelstrasse 7, D-48149, Münster, Germany. heneka@uni-muenster.de

Journal of Neuroimmunology

|January 16, 2007

Summary

Inflammation plays a key role in Alzheimer's disease (AD) pathogenesis, potentially creating a vicious cycle. Anti-inflammatory drugs show promise in reducing AD risk and delaying onset.

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Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

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Fabrication of Amyloid-β-Secreting Alginate Microbeads for Use in Modelling Alzheimer's Disease

Fabrication of Amyloid-β-Secreting Alginate Microbeads for Use in Modelling Alzheimer's Disease

Published on: July 6, 2019

Area of Science:

Neuroscience
Immunology
Pathology

Background:

Alzheimer's disease (AD) pathogenesis involves amyloid beta peptides and neurofibrillary tangles.
Neuroinflammation, involving mediators like cytokines and chemokines, is increasingly recognized as a critical factor.
Degeneration of brain stem nuclei may exacerbate inflammation in projection areas.

Purpose of the Study:

To explore the role of neuroinflammation in AD pathogenesis.
To investigate the potential of anti-inflammatory strategies for AD treatment.

Main Methods:

Review of recent evidence on inflammatory mechanisms in AD.
Analysis of the interplay between neurodegeneration and inflammation.
Examination of molecular mechanisms underlying the protective effects of anti-inflammatory drugs.

Main Results:

Inflammatory mediators can stimulate amyloid precursor protein (APP) processing, creating a detrimental cycle.
Degeneration of specific brain nuclei may promote inflammation.
Non-steroidal anti-inflammatory drugs (NSAIDs) are associated with reduced AD risk and delayed onset.

Conclusions:

Neuroinflammation is a significant contributor to AD progression and chronicity.
Targeting inflammatory pathways represents a potential therapeutic strategy for AD.
The protective effects of NSAIDs in AD may involve multiple molecular mechanisms, including inhibition of cyclooxygenase 2 (COX-2) and gamma secretase, or activation of peroxisome proliferator-activated receptor gamma (PPARγ).