{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nIn the central nervous system, neuronal pentraxin 2 (NPTX2) acts as an activity‐dependent secreted modulator that governs excitatory synapse formation and plasticity—principally by regulating the trafficking and clustering of AMPA receptor subunits (e.g. GluA4) on the postsynaptic membrane. This regulation supports proper signaling between pyramidal neurons and fast‐spiking parvalbumin‐positive interneurons, a circuit critical for maintaining network rhythmicity and cognitive function. Dysregulation of NPTX2 is evident in neurodegenerative conditions: reduced NPTX2 expression is linked to synaptic impairments and memory loss in Alzheimer’s disease, while markedly increased levels and aggregation in Parkinson’s disease (where NPTX2 is also known as Narp) as well as its misaccumulation in TDP‐43 proteinopathies further underscore its role in synaptic homeostasis. In addition, alterations of cerebrospinal fluid NPTX2 have been explored as promising biomarkers in dementia, frontotemporal dementia, and even in studies of schizophrenia and neurodevelopmental disorders, although genetic associations with autism appear limited."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn oncological contexts, NPTX2 displays context‐dependent roles that vary markedly between tumor types. In clear cell renal cell carcinoma, neuroblastoma, and cutaneous squamous cell carcinoma, overexpression of NPTX2 promotes tumor cell viability, migration, invasion, and the epithelial–mesenchymal transition—often through its interaction with AMPA receptor subunits and regulation by specific microRNAs or competing endogenous RNA networks. By contrast, in cancers such as glioblastoma, pancreatic, and gastric carcinomas, promoter hypermethylation of NPTX2 leads to its downregulation; this loss is associated with enhanced tumor progression, chemoresistance, and poorer clinical outcomes, suggesting that under some circumstances NPTX2 may function as a tumor suppressor. These divergent roles highlight the complex regulation of NPTX2 by epigenetic mechanisms and underscore its potential as both a diagnostic marker and a therapeutic target in various malignancies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "27"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nCollectively, the multifaceted functions of NPTX2—as a critical regulator of synaptic plasticity in the brain and as a context‐dependent modulator in tumor biology—underscore its broad clinical relevance. Its regulation by epigenetic modifications and noncoding RNAs, along with emerging evidence of its interplay with extracellular proteins (for example, in complex formation with coagulation factors), supports a potential role for NPTX2 as a prognostic biomarker and therapeutic target across diverse diseases. Furthermore, studies tracking CSF levels for predicting mild cognitive impairment onset and evaluations in mood disorder cohorts and frontotemporal dementia highlight the expanding translational implications of NPTX2 in both central and peripheral pathologies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "28", "end_ref": "31"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Tetsuya Marui, Shinko Koishi, Ikuko Funatogawa, et al. 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