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Updated: Sep 3, 2025
Cell-based Assay to Study Antibody-mediated Tau Clearance by Microglia
Published on: November 9, 2018
Aβ and Tau Regulate Microglia Metabolism via Exosomes in Alzheimer's Disease
Yuanxin Zhao1, Buhan Liu1, Jian Wang1
1Key Laboratory of Pathobiology, Department of Pathophysiology, Ministry of Education, College of Basic Medical Sciences, Jilin University, 126 Xinmin Street, Changchun 130021, China.
Abstract:
One of the most striking hallmarks shared by various neurodegenerative diseases, including Alzheimer's disease (AD), is microglia-mediated neuroinflammation. The main pathological features of AD are extracellular amyloid-β (Aβ) plaques and intracellular tau-containing neurofibrillary tangles in the brain. Amyloid-β (Aβ) peptide and tau protein are the primary components of the plaques and tangles. The crosstalk between microglia and neurons helps maintain brain homeostasis, and the metabolic phenotype of microglia determines its polarizing phenotype. There are currently many research and development efforts to provide disease-modifying therapies for AD treatment. The main targets are Aβ and tau, but whether there is a causal relationship between neurodegenerative proteins, including Aβ oligomer and tau oligomer, and regulation of microglia metabolism in neuroinflammation is still controversial. Currently, the accumulation of Aβ and tau by exosomes or other means of propagation is proposed as a regulator in neurological disorders, leading to metabolic disorders of microglia that can play a key role in the regulation of immune cells. In this review, we propose that the accumulation of Aβ oligomer and tau oligomer can propagate to adjacent microglia through exosomes and change the neuroinflammatory microenvironment by microglia metabolic reprogramming. Clarifying the relationship between harmful proteins and microglia metabolism will help people to better understand the mechanism of crosstalk between neurons and microglia, and provide new ideas for the development of AD drugs.
Insights
Alzheimer's disease involves neuroinflammation driven by microglia. This review proposes that amyloid-beta and tau oligomers, spread via exosomes, reprogram microglia metabolism, altering the neuroinflammatory environment.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Neuroinflammation, particularly microglia-mediated, is a hallmark of neurodegenerative diseases like Alzheimer's disease (AD).
- AD pathology involves amyloid-beta (Aβ) plaques and tau tangles, with Aβ and tau proteins as key components.
- Microglia-neuron crosstalk is crucial for brain homeostasis, and microglia metabolism influences their immune response.
Purpose of the Study:
- To explore the controversial relationship between neurodegenerative proteins (Aβ and tau oligomers) and microglia metabolism in neuroinflammation.
- To propose a mechanism by which Aβ and tau oligomers propagate and induce metabolic reprogramming in microglia.
- To highlight the role of microglia metabolic reprogramming in the neuroinflammatory microenvironment of AD.
Main Methods:
- This review synthesizes current research on microglia metabolism, neuroinflammation, and AD pathology.
- It examines the proposed role of exosomes in the propagation of Aβ and tau oligomers.
- The review focuses on the concept of microglia metabolic reprogramming as a response to these pathological proteins.
Main Results:
- Accumulation of Aβ oligomer and tau oligomer is proposed to propagate via exosomes to adjacent microglia.
- This propagation leads to microglia metabolic reprogramming, altering their function.
- The altered microglia metabolism contributes to the neuroinflammatory microenvironment characteristic of AD.
Conclusions:
- Aβ and tau oligomers can propagate through exosomes, inducing microglia metabolic reprogramming.
- Microglia metabolic reprogramming plays a key role in regulating the neuroinflammatory response in AD.
- Understanding this relationship offers new therapeutic strategies for Alzheimer's disease.
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