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Microglia and Astrocytes in Alzheimer's Disease: Significance and Summary of Recent Advances

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AGING AND DISEASE
卷 -, 期 -, 页码 -

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INT SOC AGING & DISEASE
DOI: 10.14336/AD.2023.0907

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Alzheimer's disease; microglia; astrocytes; synaptic pruning; neuroinflammation

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This article reviews the roles of microglia and astrocytes in Alzheimer's disease (AD) and emphasizes their importance in the pathogenesis and progression of AD. Research has found that these two types of glial cells play critical roles in neuroinflammation, synapse loss and pruning, clearance, and other processes related to AD. Therefore, therapeutic approaches targeting microglia and astrocytes may be promising for the treatment and prevention of AD.
Alzheimer's disease, one of the most common forms of dementia, is characterized by a slow progression of cognitive impairment and neuronal loss. Currently, approved treatments for AD are hindered by various side effects and limited efficacy. Despite considerable research, practical treatments for AD have not been developed. Increasing evidence shows that glial cells, especially microglia and astrocytes, are essential in the initiation and progression of AD. During AD progression, activated resident microglia increases the ability of resting astrocytes to transform into reactive astrocytes, promoting neurodegeneration. Extensive clinical and molecular studies show the involvement of microglia and astrocyte-mediated neuroinflammation in AD pathology, indicating that microglia and astrocytes may be potential therapeutic targets for AD. This review will summarize the significant and recent advances of microglia and astrocytes in the pathogenesis of AD in three parts. First, we will review the typical pathological changes of AD and discuss microglia and astrocytes in terms of function and phenotypic changes. Second, we will describe microglia and astrocytes' physiological and pathological role in AD. These roles include the inflammatory response, eat me and don't eat me signals, A beta seeding, propagation, clearance, synapse loss, synaptic pruning, remyelination, and demyelination. Last, we will review the pharmacological and non-pharmacological therapies targeting microglia and astrocytes in AD. We conclude that microglia and astrocytes are essential in the initiation and development of AD. Therefore, understanding the new role of microglia and astrocytes in AD progression is critical for future AD studies and clinical trials. Moreover, pharmacological, and non-pharmacological therapies targeting microglia and astrocytes, with specific studies investigating microglia and astrocyte-mediated neuronal damage and repair, may be a promising research direction for future studies regarding AD treatment and prevention.

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