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Spatial Dynamics of the Fermi Level in Electrolyte-Gated Graphene
Probing the Conformation of BamC and BamE in Native Bacterial Membranes Using Solid-State NMR Spectroscopy
Interplay of Redox Non-Innocence and Symmetry Breaking in a 4d Coordination Framework
Spatiotemporally Controlled NIR-II Afterglow Nanoprobes via Synergistic Ultrasound and Peroxynitrite-Induced Energy Transfer for Precision Theranostics
Structural Heterogeneity and Hydrodynamics of an Intrinsically Disordered Protein Condensate
Coordination-Isomerism-Driven Threshold Pressure Control of CO <sub>2</sub> and C <sub>2</sub> H <sub>2</sub> in Mixed-Ligand Switching Metal−Organic Frameworks
Beyond Thiol-Enzyme Inhibition: Sterically Bulky NHC-Au(I) Complexes are Catalytically Active Anticancer Agents with Reprogrammed Immunomodulatory Function
Dibenzocyclooctyne Conjugation Enhances Antigen Cross-Presentation and T-Cell Killing for Potent Cancer Vaccines
Enriching Local Reaction Fields via Ordered Multidimensional Interfaces for High-Yield Urea Electrosynthesis
Secondary Structure-Encoded Control of Lipid Assembly by Radially Amphiphilic Peptides
Automerization of Cyclobutadiene: Multiconfiguration Pair-Density Functional Theory Gives High Accuracy Where Unrestricted Kohn–Sham Density Functional Theory Does Not
Correction to “Detection of Mutation-Induced Conformational Changes in an Intrinsically Disordered Protein by Double Quantum Coherence Electron Spin Resonance Methodology”
Electroacupuncture-Activated Mitochondria-Targeted Polymeric Radicals for cGAS-STING-Activated Immunotherapy
Precise Optical Modulation of Charge Transport in 2D Organic Molecular Crystals through Tailor-Designed Photoswitchable Guest–Host Architectures
Chronic Pain and Cognitive Dysfunction: Clinical Implement, Mechanism, and Therapeutic Strategy
Chronic pain (CP) is increasingly recognized not only as a sensory and emotional condition but also as a significant contributor to cognitive dysfunction. Growing evidence indicates that CP-induced cognitive dysfunction arises from a cascade of neurobiological processes, including persistent neuroinflammation, neurotransmitter dysregulation, and impaired synaptic plasticity. These mechanisms particularly affect the hippocampus and medial prefrontal cortex (mPFC)—regions essential for memory, attention, and executive function. Neuroimaging studies have documented structural atrophy and disrupted network connectivity in these brain areas in CP patients. At the molecular level, pro-inflammatory cytokines such as interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) impair glutamatergic and GABAergic signaling, disrupt long-term potentiation (LTP), and inhibit neurogenesis. Additionally, dysregulation of brain-derived neurotrophic factor (BDNF) signaling exacerbates synaptic vulnerability, contributing to cognitive decline. These mechanistic overlaps are particularly relevant in aging populations and in Alzheimer's disease (AD), where CP may act as a risk factor. This review integrates clinical and preclinical findings on CP-related cognitive dysfunction, outlines key molecular mechanisms, and explores emerging therapeutic strategies targeting inflammation, neurotransmitter systems, and synaptic repair. Understanding the interaction between chronic pain and cognition is critical for developing precision treatments that address both nociceptive and neurodegenerative pathways.