Editorial: Remedying the injured brain in cognitive impairment: potential neuroimmune communication signaling and therapeutic opportunities

Nearly 16% of the global population suffers from neurological disorders linked to acute or chronic inflammation, including neurodegenerative and cerebral neuroimmune diseases (1, 2). Neuroimmune dysregulation is widely acknowledged as a pivotalmechanism in the pathogenesisof these disorders, involving intricate immune responses and cellular interactions within the central nervous system (CNS) (3). Recent advances at the intersection of neuroscience and immunology have greatly enhanced our understanding of neuroimmune signaling pathways (4). Studies have shown that resident immune cells in the brain, such as microglia and astrocytes, together with peripheral immune cells, including T cells, B cells, and monocytes, play critical roles in neuroinflammation, vascular injury, and cognitive decline (5–7). For instance, the functional states of microglia, such as the pro-inflammatory M1-type and neuroprotective M2-type polarization, as well as their transformation into disease-associated microglia, coupled with aberrant activation of the complement system, are significantly implicated in the progression of neurodegenerative diseases (8). Furthermore, the infiltration of peripheral immune cells and their communication with the CNS remain major themes in neuroimmune research (9, 10). This Research Topic brings together cutting-edge advances in neuroimmune signaling, novel microglial polarization states, peripheral immune system-to-CNS immune crosstalk, and multi-omics biomarkers associated with cognitive impairment and dementia, with a special focus on innovative therapeutic strategies targeting neuroimmune inflammation. The Research Topic includes six papers: four original research papers, one systematic review, and one opinion piece.