Neurological disorders are mainly characterized by progressive neuron loss and neurological deterioration, which cause human disability and death. However, many types of neurological disorders have similar pathological mechanisms, including the neuroinflammatory response. Various microRNAs (miRs), such as miR-21, miR-124, miR-146a, and miR-132 were recently shown to affect a broad spectrum of biological functions in the central nervous system (CNS). Microglia are innate immune cells with important roles in the physiological and pathological activities of the CNS. Recently, abnormal expression of miR-124 was shown to be associated with the occurrence and development of various diseases in CNS via regulating microglia function. In addition, miR-124 is a promising biomarker and therapeutic target. Studies on the role of miR-124 in regulating microglia function involved in pathogenesis of neurological disorders at different stages will provide new ideas for the use of miR-124 as a therapeutic target for different CNS diseases.

Traumatic brain injury (TBI) is a serious condition that poses a significant threat to human health globally. It is typically caused by direct trauma to the brain due to external forces such as impact or compression. The progression of TBI occurs in two stages based on physiological and pathological changes: primary and secondary brain injury. During the secondary stage, a large number of damage-associated molecular patterns (DAMPs) are released from injured cells into the extracellular space. These DAMPs trigger or exacerbate pathological conditions, including neuroinflammation, brain edema, diffuse axonal injury (DAI), and programmed cell death. The three main types of neural cells—neurons, microglia, and astrocytes—facilitate intercellular communication and functional crosstalk through the release and transmission of DAMPs. This forms the cellular foundation of secondary brain injury pathology. In the later stages of TBI, DAMPs are transported to various organs throughout the body via extracellular vesicles (EVs), leading to systemic changes and secondary injuries. Recent research has increasingly recognized the correlation between TBI and specific DAMPs. However, there remains a lack of comprehensive reviews exploring this relationship from a broader perspective. This review summarizes the primary pathological changes that occur after TBI, the types of DAMPs and their related signaling pathways, the role of DAMPs in mediating intercellular communication and neuronal crosstalk, the relationship between DAMPs and systemic changes following TBI. This study also highlights that DAMPs represent promising targets for the clinical diagnosis and treatment, which emphasizes the critical role of DAMPs in TBI.