Exercise Intervention Modulates Synaptic Plasticity by Inhibiting Excessive Microglial Activation via Exosomes

Li, Chen; Hu, Jijie; Liu, Wenhong; Ke, Changkai; Huang, Chuan; Bai, Yifan; Pan, Bingchen; Wang, Junyi; Wan, Chunxiao

doi:10.3389/fncel.2022.953640

Cited by 11 publications

(13 citation statements)

References 62 publications

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“…Middle cerebral artery occlusion (MCAO) damages the structure and function of synapses, resulting in neurological dysfunction. Serum exosomes from the treatment group effectively inhibited microglia activation, increased the number of synapses and the expression of plasticity‐related proteins, reduced infarct volume, and improved neural function 276,277 . Thus, exosomes can provide a new therapeutic strategy for neuroprotection and repair after stroke.…”

Section: Exosomes In Neuropsychiatric Disordersmentioning

confidence: 98%

“…Serum exosomes from the treatment group effectively inhibited microglia activation, increased the number of synapses and the expression of plasticity‐related proteins, reduced infarct volume, and improved neural function. 276 , 277 Thus, exosomes can provide a new therapeutic strategy for neuroprotection and repair after stroke. miR‐190b in ADEs inhibited apoptosis and increased neuronal survival under ischemic conditions.…”

Section: Exosomes In Neuropsychiatric Disordersmentioning

confidence: 99%

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Exosomes in brain diseases: Pathogenesis and therapeutic targets

Pang

et al. 2023

MedComm

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Exosomes are extracellular vesicles with diameters of about 100 nm that are naturally secreted by cells into body fluids. They are derived from endosomes and are wrapped in lipid membranes. Exosomes are involved in intracellular metabolism and intercellular communication. They contain nucleic acids, proteins, lipids, and metabolites from the cell microenvironment and cytoplasm. The contents of exosomes can reflect their cells’ origin and allow the observation of tissue changes and cell states under disease conditions. Naturally derived exosomes have specific biomolecules that act as the “fingerprint” of the parent cells, and the contents changed under pathological conditions can be used as biomarkers for disease diagnosis. Exosomes have low immunogenicity, are small in size, and can cross the blood–brain barrier. These characteristics make exosomes unique as engineering carriers. They can incorporate therapeutic drugs and achieve targeted drug delivery. Exosomes as carriers for targeted disease therapy are still in their infancy, but exosome engineering provides a new perspective for cell‐free disease therapy. This review discussed exosomes and their relationship with the occurrence and treatment of some neuropsychiatric diseases. In addition, future applications of exosomes in the diagnosis and treatment of neuropsychiatric disorders were evaluated in this review.

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Section: Exosomes In Neuropsychiatric Disordersmentioning

confidence: 98%

Section: Exosomes In Neuropsychiatric Disordersmentioning

confidence: 99%

Exosomes in brain diseases: Pathogenesis and therapeutic targets

Pang

et al. 2023

MedComm

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“…showed that exercise promotes the expression of synaptic plasticity‐related proteins by regulating exosomal content, which increases the number of synapses in the rat brain and thus promotes the recovery of motor function in an MCAO rat model. Moreover, subsequent experiments by Li et al 136 . demonstrated that exercise intervention regulates synaptic plasticity via inhibition of overactivated microglia via exosomes.…”

Section: Rehabilitation Therapy To Improve Synaptic Dysfunctionmentioning

confidence: 99%

“…135 showed that exercise promotes the expression of synaptic plasticity-related proteins by regulating exosomal content, which increases the number of synapses in the rat brain and thus promotes the recovery of motor function in an MCAO rat model. Moreover, subsequent experiments by Li et al136 demonstrated that exercise intervention regulates synaptic plasticity via inhibition of overactivated microglia via exosomes. Chen et al137 showed that, in an MCAO mouse model, exercise promotes synaptic proliferation and ultimately leads to nerve regeneration by converting astrocytes into neuroprotective reactive astrocytes.…”

mentioning

confidence: 99%

Current evidence of synaptic dysfunction after stroke: Cellular and molecular mechanisms

Li,

Jiang,

Fang

et al. 2024

CNS Neurosci Ther

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BackgroundStroke is an acute cerebrovascular disease in which brain tissue is damaged due to sudden obstruction of blood flow to the brain or the rupture of blood vessels in the brain, which can prompt ischemic or hemorrhagic stroke. After stroke onset, ischemia, hypoxia, infiltration of blood components into the brain parenchyma, and lysed cell fragments, among other factors, invariably increase blood–brain barrier (BBB) permeability, the inflammatory response, and brain edema. These changes lead to neuronal cell death and synaptic dysfunction, the latter of which poses a significant challenge to stroke treatment.ResultsSynaptic dysfunction occurs in various ways after stroke and includes the following: damage to neuronal structures, accumulation of pathologic proteins in the cell body, decreased fluidity and release of synaptic vesicles, disruption of mitochondrial transport in synapses, activation of synaptic phagocytosis by microglia/macrophages and astrocytes, and a reduction in synapse formation.ConclusionsThis review summarizes the cellular and molecular mechanisms related to synapses and the protective effects of drugs or compounds and rehabilitation therapy on synapses in stroke according to recent research. Such an exploration will help to elucidate the relationship between stroke and synaptic damage and provide new insights into protecting synapses and restoring neurologic function.

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“…Exercise may also regulate synaptic plasticity by promoting the migration of exosomes into the brain [ 272 ] through circulation and by preventing the overactivation of microglia [ 273 ]. Exosomes have been shown to inhibit the overactivation of M1-type microglia [ 274 , 275 ], increase the complexity of dendrites and expression of synaptic plasticity-associated proteins, and significantly reduce the volume of cerebral infarction and dysfunction.…”

Section: Therapeutic Intervention Targeting Microglia In Stroke Rehab...mentioning

confidence: 99%

The Implications of Microglial Regulation in Neuroplasticity-Dependent Stroke Recovery

2023

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Stroke causes varying degrees of neurological deficits, leading to corresponding dysfunctions. There are different therapeutic principles for each stage of pathological development. Neuroprotection is the main treatment in the acute phase, and functional recovery becomes primary in the subacute and chronic phases. Neuroplasticity is considered the basis of functional restoration and neurological rehabilitation after stroke, including the remodeling of dendrites and dendritic spines, axonal sprouting, myelin regeneration, synapse shaping, and neurogenesis. Spatiotemporal development affects the spontaneous rewiring of neural circuits and brain networks. Microglia are resident immune cells in the brain that contribute to homeostasis under physiological conditions. Microglia are activated immediately after stroke, and phenotypic polarization changes and phagocytic function are crucial for regulating focal and global brain inflammation and neurological recovery. We have previously shown that the development of neuroplasticity is spatiotemporally consistent with microglial activation, suggesting that microglia may have a profound impact on neuroplasticity after stroke and may be a key therapeutic target for post-stroke rehabilitation. In this review, we explore the impact of neuroplasticity on post-stroke restoration as well as the functions and mechanisms of microglial activation, polarization, and phagocytosis. This is followed by a summary of microglia-targeted rehabilitative interventions that influence neuroplasticity and promote stroke recovery.

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Exercise Intervention Modulates Synaptic Plasticity by Inhibiting Excessive Microglial Activation via Exosomes

Cited by 11 publications

References 62 publications

Exosomes in brain diseases: Pathogenesis and therapeutic targets

Exosomes in brain diseases: Pathogenesis and therapeutic targets

Current evidence of synaptic dysfunction after stroke: Cellular and molecular mechanisms

The Implications of Microglial Regulation in Neuroplasticity-Dependent Stroke Recovery

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