The role of microglial autophagy in Parkinson’s disease

Published on November 1, 2022

Imagine a bustling city street, where people are going about their day, each with a specific job to do. In this city, one particular group called microglia play a crucial role in maintaining peace and order. Just like the immune system keeps our bodies healthy, microglia are the guardians of the brain, protecting it from harm. However, in Parkinson’s disease, there is a disturbance in this delicate dance. A protein called α-synuclein starts piling up in the brain, disrupting the balance and triggering microglia into action. Through a process called autophagy, these vigilant cells try to eliminate the unwanted protein and restore harmony. This review delves into the intricate pathways of microglial autophagy and explores its role in Parkinson’s disease pathology. By understanding how autophagy affects microglia, scientists hope to uncover potential therapeutic targets for treating PD and restoring balance to the city of the brain.

Parkinson’s disease (PD) is the second most common neurodegenerative disease. Studies have shown that abnormal accumulation of α-synuclein (α-Syn) in the substantia nigra is a specific pathological characteristic of PD. Abnormal accumulation of α-Syn in PD induces the activation of microglia. Microglia, which are immune cells in the central nervous system, are involved in the function and regulation of inflammation in PD by autophagy. The role of microglial autophagy in the pathophysiology of PD has become a hot-pot issue. This review outlines the pathways of microglial autophagy, and explores the key factor of microglial autophagy in the mechanism of PD and the possibility of microglial autophagy as a potential therapeutic target for PD.

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