Related Experiment Video
Updated: Aug 7, 2025
Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
Published on: January 30, 2014
The effects of microglia-associated neuroinflammation on Alzheimer's disease
Cuicui Wang1, Shuai Zong1, Xiaolin Cui2
1Department of Clinical Laboratory Medicine, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Abstract:
Alzheimer's disease (AD) is defined as a severe chronic degenerative neurological disease in human. The pathogenic mechanism of AD has been convincingly elucidated by the "amyloid cascade hypothesis" with the main focus of the pathological accretion of β-amyloid (Aβ) peptides outside the cell. However, increasing evidence suggests that this hypothesis is weak in explaining the pathogenesis of AD. Neuroinflammation is crucial in the development of AD, which is proven by the elevated levels of inflammatory markers and the identification of AD risk genes relevant to the innate immune function. Here, we summarize the effects of microglia-mediated neuroinflammation on AD, focusing on the temporal and spatial changes in microglial phenotype, the interactions among microglia, Aβ, tau, and neurons, and the prospects and recent advances in neuroinflammation as a diagnostic and therapeutic target of AD.
Insights
Neuroinflammation, driven by microglia, plays a key role in Alzheimer's disease (AD) pathogenesis. Understanding microglial changes and their interactions offers new diagnostic and therapeutic avenues for AD.
Area of Science:
- Neuroscience
- Immunology
- Neuropathology
Background:
- Alzheimer's disease (AD) is a chronic neurodegenerative disorder.
- The amyloid cascade hypothesis, focusing on beta-amyloid (Aβ) plaques, has limitations in explaining AD pathogenesis.
- Emerging evidence highlights the critical role of neuroinflammation in AD development.
Purpose of the Study:
- To summarize the impact of microglia-mediated neuroinflammation on Alzheimer's disease.
- To explore the dynamic changes in microglial phenotypes.
- To review interactions between microglia, Aβ, tau, and neurons in AD.
Main Methods:
- Review of current literature on neuroinflammation in Alzheimer's disease.
- Analysis of temporal and spatial changes in microglial phenotypes.
- Examination of molecular and cellular interactions in AD pathology.
Main Results:
- Microglia activation and altered phenotypes are central to AD progression.
- Neuroinflammation significantly influences the interplay between Aβ, tau pathology, and neuronal dysfunction.
- Elevated inflammatory markers and AD risk genes linked to innate immunity confirm neuroinflammation's role.
Conclusions:
- Neuroinflammation, particularly microglia-mediated, is a critical factor in Alzheimer's disease.
- Targeting microglial pathways presents promising diagnostic and therapeutic strategies for AD.
- Further research into neuroinflammation offers new hope for combating AD.
More Related Videos
10:40Immunofluorescence Staining Using IBA1 and TMEM119 for Microglial Density, Morphology and Peripheral Myeloid Cell Infiltration Analysis in Mouse Brain
Published on: October 27, 2019
08:47Author Spotlight: In Vitro Co-Culture Model for Studying Microglia-Neuronal Interactions in Disease Conditions
Published on: July 26, 2024
Related Concept Videos
01:26Alzheimer's Disease: Overview
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
01:22Alzheimer's Disease: Treatment