Abstract
Microglia play an important role in neurodegenerative disease [i.e., Parkinson’s disease (PD), Alzheimer’s disease (AD), and amyotrophic lateral sclerosis (ALS)]. These diseases share some similar pathological changes and several microglia-associated processes, including immune response, neuroinflammation, phagocytosis, elimination of synapses et al. Microglia in the central nervous system (CNS) has been described as having both destructive and protective effects in neurological disorders. Besides, considerable evidence also indicates that microglia play a significant role in neurogenesis, neuronal cell death, and synaptic interactions. The communication between microglia and neurons is of vital role in regulating complex functions which are key to appropriate the activity of the brain. Accumulating studies have also demonstrated that exosomes with sizes ranging from 40–100 nm, released by microglia, could serve as key mediators in intercellular signaling. These exosomes, identified in terms of cellular origin in many kinds of biological fluids, exert their effects by delivering specific cargos such as proteins, microRNAs (miRNAs), and mRNAs. It was shown that microglial exosomes could transport to and be uptake by neurons, which may either be beneficial or instead, detrimental to CNS diseases. The focus of this review is to summarize the involvement of microglial exosomes in critical pathologies associated with neurodegenerative disease and how they contribute to these disorders, including PD, AD, and ALS. We also review the application of microglia exosomes as potential biomarkers in monitoring disease progression, as well as focusing on their roles as drug delivery vehicles in treating neurodegenerative disorders.
Highlights
The communication between diverse cellular populations is a characteristic of neurodegenerative disorders, with different ways including exocytosis, exosomes, tunneling nanotubes, and endocytosis (Fruhbeis et al, 2013; Peferoen et al, 2014; Valdinocci et al, 2017)
MicroRNAs, messenger RNAs, proteins, and cytokines can be selectively incorporated into multivesicular bodies (MVBs) and secreted from microglia encapsulated in exosomes
We found that inhibition of dynamin-related protein (Drp-1), a protein known for its function in mitochondrial fission, could enhance autophagy flux and inhibit α-syn carrying exosomes release, reducing microglia to neuron transmission and α-syn aggregation in neurons (Fan et al, 2019)
Summary
Min Guo1†, Yining Hao1†, Yiwei Feng, Haiqing Li2, Yiting Mao, Qiang Dong3* and Mei Cui1*. Microglia play an important role in neurodegenerative disease [i.e., Parkinson’s disease (PD), Alzheimer’s disease (AD), and amyotrophic lateral sclerosis (ALS)] These diseases share some similar pathological changes and several microglia-associated processes, including immune response, neuroinflammation, phagocytosis, elimination of synapses et al Microglia in the central nervous system (CNS) has been described as having both destructive and protective effects in neurological disorders. Accumulating studies have demonstrated that exosomes with sizes ranging from 40–100 nm, released by microglia, could serve as key mediators in intercellular signaling These exosomes, identified in terms of cellular origin in many kinds of biological fluids, exert their effects by delivering specific cargos such as proteins, microRNAs (miRNAs), and mRNAs. It was shown that microglial exosomes could transport to and be uptake by neurons, which may either be beneficial or instead, detrimental to CNS diseases.
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