Neurological disorders represent one of the most pressing challenges in contemporary medicine, requiring tools that enable early diagnosis, targeted treatment, and deeper mechanistic understanding. Conventional biological agents such as antibodies, though widely used, often face limitations related to stability, brain penetration, cost, and integration into real-world platforms. Molecularly imprinted polymers (MIPs) have emerged as a promising synthetic alternative, capable of mimicking the molecular recognition functions of biological systems while offering enhanced robustness and customisability. MIPs provide key advantages, including high thermal and chemical stability, reusability, and design flexibility, making them especially attractive for neurological applications. In this review, we begin by presenting an overview of the main MIP formats applied in neurology, detailing their preparation, characterisation, and application-relevant advantages and limitations. We then explore the most actively investigated areas of MIP use in neurological diagnostics, research, and therapy, with a particular focus on: (i) nerve agents, (ii) neurotransmitters, and biomarkers, and (iii) drug development, drug delivery, and direct biological activity. Finally, we discuss the key challenges that currently hinder the clinical translation of MIPs in neurology, including poor biodegradability, in vivo biocompatibility concerns, and scalability, along with emerging strategies aimed at overcoming these barriers. We hope this analysis will serve as a useful reference for neuroscientists seeking novel material-based tools, as well as for materials scientists aiming to develop neurological applications of molecular imprinting.

Facial expression recognition (FER) has emerged as a pivotal interdisciplinary research domain that bridges computer science, psychology, neuroscience, and medicine. By mapping the FER scientific knowledge graph, this study aimed to explore the technological evolution and forecast future trends in this field. The study collected and cleaned the research on emotion perception in the Web of Science (WoS) database, and utilized the software CiteSpace (version 6.4R1) and R (BiblioShiny packages) software to create a scientific knowledge map. K-means was used for cluster analysis, and then the latent Dirichlet allocation (LDA) was employed to extract popular topics from the text of each cluster. Uniform manifold approximation and projection (UMAP) was utilized to reduce high-dimensional embeddings to a two-dimensional space. From a regional perspective, research is mainly distributed in countries or regions such as North America, Western Europe, East Asia, India, and Australia. Research on facial emotion recognition has focused primarily on neuroscience, psychiatry, and psychology. With the rapid development of computer technology, the interdisciplinary intersection is becoming increasingly important as FER has shown strong potential in identifying rare and neurological diseases. Furthermore, the evolution of artificial intelligence (AI) has transformed facial expression feature extraction from manual methodologies to machine learning-based approaches. The rapid development of computer algorithms and AI has greatly improved the accuracy and speed of facial emotion recognition. As a technology capable of detecting instantaneous emotional changes, FER holds promising prospects in fields such as neuroscience, emotion analysis, and pain assessment.

Alzheimer's disease (AD) pathogenesis is characterized by the accumulation of amyloid beta (Aβ) deposits in the cerebral parenchyma and vasculature, a condition referred to as cerebral amyloid angiopathy (CAA). Besides the full-length form, Aβ deposits showed a highly heterogenous composition due to the action of different proteolytic enzymes. N-terminal Aβ peptides have shown higher aggregation propensity and toxicity compared to the other truncated forms, with species starting at residue phenylalanine 4 (Aβ4-x) being more neurotoxic than the others. Thus, Aβ4-x species have drawn attention in AD pathogenesis, potentially offering novel therapeutic targets to halt or reverse disease progression. Antibodies targeting specifically Aβ4-x species were designed with the aim of preventing their aggregation and promoting their clearance counterbalancing their neurotoxic effect. This work provides an update on monoclonal and polyclonal antibodies developed to specifically target Aβ4-x species in AD and CAA preclinical studies (in vitro and in vivo models).

Chemotherapy-induced peripheral neuropathy (CIPN) is a common complication in patients with malignant tumors during chemotherapy. The pathological mechanisms of CIPN remain unclear, and effective preventive and therapeutic strategies are still lacking, posing a major challenge in clinical practice. Aberrant activation of spinal glial cells, particularly microglia and astrocytes, is a key pathological hallmark of CIPN. Evidence from multiple animal models supports a causal link between glial activation and CIPN, suggesting that glial cells may serve as potential therapeutic targets. However, owing to the diversity of chemotherapy agents, the mechanisms of glial activation in CIPN differ and remain insufficiently characterized. This review takes spinal glial activation induced by peripheral nerve injury as its starting point, with a specific focus on microglia and astrocytes. It provides a systematic overview of their roles and mechanisms in CIPN caused by commonly used chemotherapeutic agents. The aim is to deepen understanding of CIPN pathogenesis and provide a foundation for developing targeted therapies.

Obsessive-compulsive disorder (OCD) is a common and disabling, as well as underdiagnosed, neuropsychiatric condition characterized by involuntary and unwanted obsessions and/or compulsions, often accompanied by states of severe anxiety, distress and shame, as well as other comorbid disorders. Despite the extensive literature available to date, only some of the neurobiological mechanisms underlying the symptomatic manifestations of the disorder have been clarified, underlining the need for further research. The brain structures involved are hippocampus, amygdala, striatum, thalamus, dorsolateral prefrontal cortex, anterior cingulate cortex, and orbitofrontal cortex; furthermore, most studies have mainly focused on the expressive modalities and on the individual structural and functional alterations of the brain, generating sometimes conflicting data. The aim of this article is therefore to summarize and bring together the main evidence collected so far on what would appear to be the neuroanatomical correlates and mechanisms underlying the disorder and its manifestations, to provide a sufficiently clear and complete overview.

Cranial-irradiation is associated with tissue damage resulting in neurocognitive impediments that adversely influence patient quality of life. Administration of radiation directly to the tumor may extend to the neighboring healthy tissues, which may induce acute to persistent oxidative stress, lessening neurogenesis, neuroinflammation, as well as vascular alterations, leading to neurocognitive sequelae as a result of decline in neuronal structural complexity as well as synaptic connections. Almost all the medications indicated in the treatment of irradiation-triggered brain injury work via signaling pathways that are associated with lessening chronic oxidative stress, which is considered a consequence of the inflammatory response, reduction of edema, as well as microglia activation. Some agents have both preventative as well as therapeutic potential via the amalgamation of both neuroprotective and therapeutic mechanisms above. Thus, in this review, agents such as baicalein, troxerutin, epigallocatechin gallate, quercetin, melatonin, valproic acid, lithium, neurosteroid progesterone as well as minocycline have been implicated as neuroprotective agents for irradiation-induced neurological deficits. Also, agents such as glucocorticoids, methylphenidate, vitamin E, bisdemethoxycurcumin, phosphodiesterases, edaravone, pioglitazone and fenofibrate, glutamate antagonists, human urinary kallidinogenase, bevacizumab, as well as hyperbaric oxygen have been implicated as therapeutic agents for irradiation-induced neurological deficits. Furthermore, agents such as angiotensin-converting enzyme, 3-N-butyl-phthalide, stem cell therapy, sphingosine-1-phosphate, gangliosides, and neurotrophins have been implicated as combined potential neuroprotective and therapeutic agents for irradiation-induced neurological deficits. The aim of this review is to elucidate the potential neuroprotective and therapeutic agents above and their mechanisms for irradiation-induced neurological deficits after brain irradiation.

Visual impairment has been recognized as a potential risk factor for depressive symptoms (DS) in diabetes patients, yet the role of visual function in predicting DS remains unexplored. This study aims to develop and validate a predictive model for DS risk in type 2 diabetes mellitus (T2DM) patients in community health settings, incorporating a visual function index (VF14). We conducted a cross-sectional study involving 542 T2DM patients from four community health centers in Guiyang. Univariate and multivariate logistic regressions identified significant predictors, while 10 machine learning algorithms were employed to construct the predictive model. Model performance was assessed using such metrics as receiver operating characteristic curves, accuracy, sensitivity, specificity, F1 score, Brier score, C-index, calibration curves, and decision curve analysis. A restricted cubic spline (RCS) analysis evaluated the score-dependent risk profiles between the VF14 and DS. Key predictors included body mass index (BMI), self-reported glycemic status, age-related macular degeneration, glycated hemoglobin (HbA1c), and VF14. Among the models, the gradient boosting machine exhibited the robust predictive performance, with an area under the curve of 0.73 and sensitivity of 0.72. The Shapley additive explanations analysis identified VF14, BMI, and HbA1c as the top risk factors. RCS analysis revealed a score-dependent risk profile between VF14 and DS risk. This study introduces a clinically interpretable tool for early DS risk stratification in T2DM patients, offering potential for improved risk assessment and timely intervention in community health settings.

Traumatic brain injury (TBI) causes significant mortality. Dexmedetomidine (DEX) shows neuroprotective potential in animals, but clinical evidence remains inconsistent. We evaluated the impact of early DEX, initiated within 48 h of admission with a treatment duration of at least 4 h, on survival in intensive care unit (ICU) patients with TBI using the Medical Information Mart for Intensive Care-IV (MIMIC-IV) database. Outcomes included 28-day, hospital, and 1-year mortality, analyzed via propensity score matching (PSM), multivariable Cox models, and subgroup analyses. Of 2378 patients, 241 received DEX. After PSM (235 pairs), early DEX use significantly reduced 28-day (HR 0.45, 95% CI 0.30–0.69, p < 0.001) and hospital mortality (HR 0.25, 95% CI 0.15–0.42, p < 0.001). These results remained robust across sensitivity analyses. Similarly, 1-year mortality decreased (HR 0.64, 95% CI 0.47–0.87, p < 0.01) and further supported by the Boruta algorithm, although inverse probability of treatment weighting analysis showed only a non-significant trend (p = 0.08). Survival benefits were more pronounced in patients aged <65 and those requiring mechanical ventilation. In conclusion, early DEX use is associated with improved short- and long-term survival in ICU patients with TBI, particularly in younger individuals and those requiring mechanical ventilation. Randomized controlled trials are warranted to establish causality.

Triple-therapy regimens involving Pregabalin or Gabapentin with nortriptyline and Methylcobalamin have been shown to be efficacious in treating neuropathic pain in clinical trials. This study aims to compare the clinical effectiveness and treatment satisfaction of two triple-therapy regimens in treating neuropathic pain in a real-world setting. This prospective, single-center, observational study compared the efficacy, safety, and treatment satisfaction of triple therapy in Pregabalin triple therapy versus Gabapentin triple therapy for patients with neuropathic pain. The primary outcome measured the reduction in mean Self-Administered Leeds Assessment of Neuropathic Symptoms and Signs pain score value from the baseline to 12 weeks posttreatment. The secondary outcome measured the treatment satisfaction for both therapies using the Treatment Satisfaction Questionnaire for Medication version 1.4. Of 264 patients who received either treatment group, during the third follow-up, it became evident that Group A Pregabalin triple therapy yielded a significantly more substantial reduction in neuropathic pain (60.61%) when compared to Group B Gabapentin triple therapy (12.88%). Furthermore, patients expressed markedly higher levels of satisfaction and convenience with the Pregabalin treatment (p ≤ 0.001). Our study's findings, encompassing both clinical effectiveness and treatment satisfaction, unequivocally demonstrate that Group A surpasses Group B in ameliorating neuropathic symptoms and signs. Pregabalin is a more effective and convenient treatment for neuropathic pain than Gabapentin, with no significant difference in side effects. Clinicians should consider Pregabalin as a first-line treatment option for neuropathic pain, especially for patients not responding to Gabapentin or who seek a more convenient option.