Extracellular vesicles (EVs), diverse membranous vesicles secreted by cells, include microvesicles, exosomes, and other cell-specific types. They efficiently deliver proteins and nucleic acids to distal parts and are implicated in the pathology of neurodegenerative disorders. Additionally, long-term exposure to extracellular microparticles, notably particulate matter (PM) 2.5, is suspected to induce neuroinflammation via oxidative stress mechanisms. Production of macrovesicles relies on the ARRDC1 and ARF6/RhoA pathways, whereas exosome production involves both ESCRT-dependent and ESCRT-independent pathways. In neurodegenerative disorders, EVs play various roles: microglia-derived EVs activate endothelial cells and neurons in stroke models, EVs accelerate α-synuclein aggregation and hinder autophagy in Parkinson's disease, patient-derived muscle cell small Extracellular vesicles (sEVs) worsen motor neuron death in Amyotrophic lateral sclerosis (ALS), and microglia-derived EVs influence neuronal transmission through the hippocampus, leading to synaptic spine reduction in Alzheimer's disease. However, the precise mechanisms underlying the involvement of EVs in disease onset remain largely unknown, emphasizing the need for further investigations.

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Neurodegenerative Disorder and Fine Particulate Matter

  • Hironori Kawahara,
  • Rikinari Hanayama

摘要

Extracellular vesicles (EVs), diverse membranous vesicles secreted by cells, include microvesicles, exosomes, and other cell-specific types. They efficiently deliver proteins and nucleic acids to distal parts and are implicated in the pathology of neurodegenerative disorders. Additionally, long-term exposure to extracellular microparticles, notably particulate matter (PM) 2.5, is suspected to induce neuroinflammation via oxidative stress mechanisms. Production of macrovesicles relies on the ARRDC1 and ARF6/RhoA pathways, whereas exosome production involves both ESCRT-dependent and ESCRT-independent pathways. In neurodegenerative disorders, EVs play various roles: microglia-derived EVs activate endothelial cells and neurons in stroke models, EVs accelerate α-synuclein aggregation and hinder autophagy in Parkinson's disease, patient-derived muscle cell small Extracellular vesicles (sEVs) worsen motor neuron death in Amyotrophic lateral sclerosis (ALS), and microglia-derived EVs influence neuronal transmission through the hippocampus, leading to synaptic spine reduction in Alzheimer's disease. However, the precise mechanisms underlying the involvement of EVs in disease onset remain largely unknown, emphasizing the need for further investigations.