Neurotherapeutics最新文献

{"title":"Immunosenescence as a modifiable driver of neurodegenerative diseases: Pathways and multidimensional emerging strategies for Alzheimer's and Parkinson's diseases","authors":"Jingyu Zhao,&nbsp;Linzhuo Qu,&nbsp;Hongjian Guan,&nbsp;Huiying Che,&nbsp;Fei Shi,&nbsp;Yang Yang","doi":"10.1016/j.neurot.2026.e01096","DOIUrl":"10.1016/j.neurot.2026.e01096","url":null,"abstract":"<div><div>Immunosenescence represents a core upstream driver of Alzheimer's disease (AD) and Parkinson's disease (PD), exerting its pathological effects through four mechanistically interconnected cascades: chronic inflammatory imbalance mediated by the senescence-associated secretory phenotype (SASP), oxidative stress arising from immune-metabolic reprogramming, protein homeostasis dysfunction caused by autophagy-lysosomal failure, and disrupted neuro-immune crosstalk secondary to breakdown of central nervous system (CNS) immune privilege. Current clinical practice remains largely constrained to neurotransmitter-based symptomatic management, which can neither arrest upstream pathological progression nor restore lost neuronal populations. Emerging intervention strategies targeting immunosenescence, including senolytic agents, antioxidant and metabolic modulators, autophagy restoration, and precision-targeted nanocarrier delivery, have demonstrated substantial capacity to delay disease progression in preclinical and early clinical investigations. These strategies act through selective clearance of senescent immune cells, remodeling of the neuroinflammatory microenvironment, and restoration of cellular quality-control mechanisms. The multidimensional treatment strategy approaches from the perspectives of artificial intelligence (AI) guided target discovery, nanocarrier engineering, and gut microbiota intervention to simultaneously address multiple nodes in the immunosenescence network, thereby overcoming the inherent limitations of single-target strategies. This review consolidates current mechanistic evidence and translational data to establish immunosenescence as an actionable therapeutic target and to provide a conceptual framework for precision disease-modifying therapy in AD and PD.</div></div>","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":"23 6","pages":"Article e01096"},"PeriodicalIF":7.4,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149166198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gabapentin and cognitive impairment after traumatic brain injury: A multinational cohort of 49,925 patients","authors":"Isaac B. Thorman,&nbsp;Ariel Sacknovitz,&nbsp;Anjali Goyal,&nbsp;Austin G. Li,&nbsp;Aryan Malhotra,&nbsp;Eric Feldstein,&nbsp;Jude Al-Mufti,&nbsp;Patricia E. McGoldrick,&nbsp;Michael C. Schubert,&nbsp;Carrie R. Muh,&nbsp;Dennis J. Keselman,&nbsp;Mill Etienne,&nbsp;Steven M. Wolf,&nbsp;Tatyana R. Gitlevich,&nbsp;Merritt D. Kinon,&nbsp;Jon B. Rosenberg,&nbsp;Andrew Bauerschmidt,&nbsp;Saef Izzy,&nbsp;Stephan A. Mayer,&nbsp;Chirag D. Gandhi,&nbsp;Fawaz Al-Mufti","doi":"10.1016/j.neurot.2026.e01041","DOIUrl":"10.1016/j.neurot.2026.e01041","url":null,"abstract":"<div><div>Traumatic brain injury (TBI) is a major cause of morbidity and mortality, and cognitive impairment can be devastating among survivors. The objective was to assess an association between gabapentin and cognitive impairment after TBI. This retrospective cohort study used the multinational TriNetX Research Network (&gt;150 million patients). Adults (≥18 years) with a first TBI and Glasgow Coma Scale (GCS) score recorded on the day of injury were included. Patients with known cognitive impairment or gabapentin exposure were excluded. The cohort (<em>n</em> = 49,925) was stratified into mild (GCS 13–15; <em>n</em> = 34,376), moderate (9–12; <em>n</em> = 4035), and severe (3–8; <em>n</em> = 12,845) TBI. The risk of cognitive impairment and mortality were assessed using Cox proportional hazard models adjusted for known predictors. Secondary analyses examined levetiracetam use (as seizure prophylaxis) and long-term medical and functional outcomes. Among 49,925 included patients w, 3.5% received gabapentin on the day of TBI. After adjustment, gabapentin was associated with a 22% lower risk of cognitive impairment in mild TBI (HR = 0.78; 95% CI, 0.62–0.98; <em>P</em> = .03) and a 46% lower risk of mortality in severe TBI (HR = 0.54; 95% CI, 0.40–0.72; <em>P</em> &lt; .001). Levetiracetam showed no protective association with cognition. Long-term follow-up associated gabapentin use with lower mortality but higher rates of psychiatric/sleep diagnoses, reduced mobility, atrial fibrillation, and pulmonary embolism. Although causality cannot be inferred, these findings suggest gabapentin warrant prospective investigation as a candidate neuroprotective therapy.</div></div>","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":"23 5","pages":"Article e01041"},"PeriodicalIF":7.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148765076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Wild-type C9orf72 drives proteasomal dysfunction and mutant aggregates via a Stat1-Isg15 axis in Huntington’s disease","authors":"Siew Chin Chan,&nbsp;Chih-Wei Tung,&nbsp;Chih-Yi Chang,&nbsp;Ching-Chun Su,&nbsp;Yi-Ching Chen,&nbsp;Po-Ming Wu,&nbsp;Chia-Yu Tung,&nbsp;Shih-Feng Chen,&nbsp;Hsiao-Ying Kuo,&nbsp;Pei-Hsun Cheng,&nbsp;Chuan-Mu Chen,&nbsp;Shang-Hsun Yang","doi":"10.1016/j.neurot.2026.e00970","DOIUrl":"10.1016/j.neurot.2026.e00970","url":null,"abstract":"<div><div>Mutant C9orf72 has been extensively studied as a major genetic cause of amyotrophic lateral sclerosis and frontotemporal dementia, and is also known to generate Huntington’s disease (HD)-like phenocopies. However, despite this strong disease association, the role of wild-type C9orf72 (wt-C9orf72) in neurodegeneration remains largely unexplored. HD is a neurodegenerative disease, and characterized by the accumulation of misfolded mutant Huntingtin (mHTT) and impaired proteostasis, yet the upstream mechanisms driving ubiquitin-proteasome system (UPS) dysfunction are not fully understood. Here, we identify a previously unrecognized modulatory role of wt-C9orf72 in regulating mHTT aggregation in experimental HD models. Analysis of public transcriptomic datasets reveal context-dependent C9ORF72 expression changes across HD-related human datasets, while C9orf72 levels are increased in R6/2 mouse brain lysates. Functional analyses reveal that overexpression of wt-C9orf72 increases mHTT aggregation and is accompanied by increased apoptotic signaling and reduced cell viability. Unbiased proteomic profiling identifies Stat1 as a key downstream effector. Mechanistically, wt-C9orf72 promotes Stat1 activation and nuclear translocation, leading to transcriptional upregulation of Isg15, a ubiquitin-like modifier. Elevated Isg15 disrupts UPS function, resulting in accumulation of polyubiquitinated proteins and impaired proteasomal degradation. Importantly, genetic suppression of Stat1 or Isg15 significantly attenuates C9orf72-associated mHTT aggregation, supporting a functional C9orf72-Stat1-Isg15 axis. Consistent with these cell-based findings, Stat1, phosphorylated Stat1 and Isg15 levels are elevated in the cortex and striatum of R6/2 HD mouse brains. Collectively, our findings identify a novel wt-C9orf72-Stat1-Isg15 axis that promotes proteasomal dysfunction and mHTT aggregation, providing new insights into wt-C9orf72-associated protein homeostasis.</div></div>","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":"23 5","pages":"Article e00970"},"PeriodicalIF":7.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148685001","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Use of nucleoside therapy for mitochondrial DNA depletion/deletion syndrome (MDDS)","authors":"Michio Hirano,&nbsp;Andres Berardo,&nbsp;Emanuele Barca,&nbsp;Valentina Emmanuele,&nbsp;Austin Larson,&nbsp;Antonella Spinazzola,&nbsp;Amel Karaa","doi":"10.1016/j.neurot.2026.e01048","DOIUrl":"10.1016/j.neurot.2026.e01048","url":null,"abstract":"","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":"23 5","pages":"Article e01048"},"PeriodicalIF":7.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148795971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pharmacological actions of novel beta-lactam and non-beta lactam compounds on major astrocytic glutamate transporters in the brain and liver of male C57BL/6 mice exposed chronically to hydrocodone","authors":"Woonyen Wong,&nbsp;Adil Shareef Mohammed,&nbsp;Wayne E. Childers,&nbsp;Magid Abou-Gharbia,&nbsp;Youssef Sari","doi":"10.1016/j.neurot.2026.e01071","DOIUrl":"10.1016/j.neurot.2026.e01071","url":null,"abstract":"<div><div>Chronic exposure to opioid reduced the expression of astrocytic glutamate transporter 1 (GLT-1) and cystine/glutamate antiporter (xCT) in the mesocorticolimbic brain region and ceftriaxone, a beta-lactam antibiotic, attenuated this effect. Importantly, a novel synthetic non-antibiotic beta-lactam, MC-100093, was found effective in attenuating fentanyl and morphine overdose-induced reduction in GLT-1 expression in the nucleus accumbens (NAc) as well as attenuated fentanyl-induced liver inflammation and disruption of liver metabolites. In the present study, two novel synthetic non-antibiotic beta-lactams, MC-100093 and MC-290401, and one novel synthetic non-beta-lactam bicyclic, MC-290013, were tested in a mouse model of chronic exposure to hydrocodone with focus on GLT-1 expression as well as the transcriptional regulation of GLT-1. This study reports that MC-100093, MC-290401, and MC-290013 treatment attenuated hydrocodone-induced downregulation of GLT-1 in the NAc. MC-100093, MC-290401, and MC-290013 treatments normalized GLT-1 and xCT expression in the NAc, and this effect was associated with upregulation of NFκB in the nuclear fraction and downregulation of the expression of mTOR and IKB-α in the cytoplasmic fraction as well as upregulation of pAkt expression in the NAc. Furthermore, histological and statistical analyses revealed that MC-100093, MC-290401, and MC-290013 treatments attenuated chronic hydrocodone-induced liver inflammation (TNF-α, IL-1β, and IL-6). Finally, these GLT-1 modulators attenuated hydrocodone-induced upregulation of hepatic xCT and GLT-1. These findings suggest that these novel synthetic GLT-1 modulators may be considered as potential agents to attenuate hydrocodone-induced alterations in glutamate transporters and associated target proteins in the brain and liver.</div></div>","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":"23 5","pages":"Article e01071"},"PeriodicalIF":7.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148930764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stimulation selectively blocks subthalamic high β–cortical high γ coupling in Parkinson’s disease","authors":"Ádám József Berki,&nbsp;Hao Ding,&nbsp;Marcell Palotai,&nbsp;László Halász,&nbsp;Loránd Erőss,&nbsp;Gábor Fekete,&nbsp;László Bognár,&nbsp;Andrea Kelemen,&nbsp;Borbála Jávor-Duray,&nbsp;Éva Pichner,&nbsp;Avin Aphrodite Babakhani,&nbsp;Muthuraman Muthuraman,&nbsp;Gertrúd Tamás","doi":"10.1016/j.neurot.2026.e01059","DOIUrl":"10.1016/j.neurot.2026.e01059","url":null,"abstract":"<div><div>Subthalamic stimulation in Parkinson’s disease may operate by suppressing high-beta connectivity along the hyperdirect pathway and by promoting gamma motor cortical processing. We examined how the phase of beta activity shapes the amplitude of the gamma rhythm along hyperdirect connections and how stimulation influences this coupling. Thirty-eight patients with akinetic-rigid Parkinson’s disease treated with bilateral subthalamic stimulation were recruited. A high-density electroencephalogram was recorded at rest and while patients drew self-paced and traced spirals on a digital tablet at four stimulation levels. We analyzed time-resolved phase-amplitude coupling between low (13–20 Hz) and high beta (21–30 Hz) and low (31–60 Hz) and high gamma (61–100 Hz) frequency band pairs between the subthalamic nucleus and motor cortical areas. The stimulation-induced decreases in phase-amplitude coupling were correlated with real-time improvement in bradykinesia and predicted by clinical factors. Among the subthalamic beta–cortical gamma bands, the high beta–high gamma phase-amplitude coupling was the largest (p &lt; 0.001), and decreased the most at the highest stimulation level (p &lt; 0.001), in correlation with the improvement in bradykinesia. Its stimulation-induced decrease could be predicted in task-specific pathways consisting of the primary motor cortex and the dorsal premotor cortex; the rate of improvement in drawing speed and the active contact locations were the key predictors. Phase–amplitude coupling of the cortical beta–subthalamic gamma band pairs did not respond to stimulation. Subthalamic stimulation selectively interferes with the subthalamic high beta-driven cortical gamma block in task-specific pathways in Parkinson’s disease, tracking the improvements in bradykinesia.</div></div>","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":"23 5","pages":"Article e01059"},"PeriodicalIF":7.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148887697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Striatal temporal interference stimulation alleviates motor deficits and confers neuroprotection in an MPTP-induced mouse model of Parkinson’s disease with associated improvements in mitochondrial homeostasis","authors":"Jin Peng,&nbsp;Ziyu Wang,&nbsp;Yu Liu,&nbsp;Xiaohui Wang","doi":"10.1016/j.neurot.2026.e01064","DOIUrl":"10.1016/j.neurot.2026.e01064","url":null,"abstract":"<div><div>Temporal interference (TI) stimulation is an emerging noninvasive neuromodulation approach capable of selectively targeting deep brain structures, but its therapeutic effects and underlying mechanisms in Parkinson’s disease (PD) remain unclear. Here, we evaluated striatal TI stimulation in an MPTP-induced mouse model of PD. TI stimulation using 2 and 2.02 kHz carrier frequencies, a 20 Hz offset, and a current of 150 μA was delivered for 10 min/day, with 30 s ramp-up and ramp-down, for 7 or 14 consecutive days. We found that TI stimulation significantly reduced motor deficits, with greater behavioral benefit observed after 14 days of stimulation, and attenuated dopaminergic neurodegeneration and α-synuclein accumulation. Meanwhile, TI stimulation improved multiple aspects of mitochondrial homeostasis, including mitochondrial morphology and dynamics, PINK1/Parkin-mediated mitophagy, complex I activity, and mitochondria-dependent apoptotic signaling. Importantly, pharmacological inhibition with Mdivi-1 largely attenuated the behavioral, neuropathological, and mitochondrial effects of TI stimulation, suggesting that mitochondrial quality-control pathways may contribute to TI-associated neuroprotection. Together, these findings indicate that striatal TI stimulation ameliorates motor impairment and exerts neuroprotective effects in parkinsonian mice, with associated improvements in mitochondrial homeostasis, and support TI stimulation as a promising noninvasive therapeutic strategy for PD.</div></div>","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":"23 5","pages":"Article e01064"},"PeriodicalIF":7.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148913050","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrative transcriptomic analysis reveals KLHL2 downregulation as a potential driver of microglial inflammation in Alzheimer’s disease via the WNK3/JNK/c-Jun axis","authors":"Yao Yang,&nbsp;Conghui Dai,&nbsp;Zongtang Xu,&nbsp;Linpei Zhuo,&nbsp;Kun Xiang,&nbsp;Xiaoou Lin,&nbsp;Jing Sun,&nbsp;Jiaming Liu,&nbsp;Qiuling Tong","doi":"10.1016/j.neurot.2026.e01069","DOIUrl":"10.1016/j.neurot.2026.e01069","url":null,"abstract":"<div><div>Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by prominent neuroinflammation. Microglia, the resident immune cells of the central nervous system, play a key role in AD-associated neuroinflammation, yet the molecular mechanisms regulating their inflammatory activation remain incompletely understood. In this study, we integrated human single-nucleus RNA sequencing with computational analyses and experimental validation to identify potential regulators of inflammatory microglial states in AD. Microglial subpopulations were characterized, and pseudotime analysis was performed to infer transcriptional state transitions across neuropathological stages. High-dimensional weighted gene co-expression network analysis (hdWGCNA) and machine learning were used to prioritize candidate genes for functional validation. <em>KLHL2</em> was identified as a candidate regulator, and its expression progressively decreased along the inferred pseudotime trajectory, with concordant decreases in <em>Klhl2</em> mRNA and KLHL2 protein levels observed in APP/PS1 mice and Aβ42-stimulated BV2 cells. In contrast, WNK3 expression level increased without corresponding changes in <em>Wnk3</em> mRNA. In BV2 cells, <em>Klhl2</em> overexpression reduced WNK3 expression level, JNK and c-Jun phosphorylation, and pro-inflammatory mediator expression, whereas <em>Klhl2</em> knockdown produced the opposite effects. Collectively, these findings support KLHL2 as a negative regulator of microglial inflammatory activation and suggest the involvement of WNK3/JNK/c-Jun signaling in this process.</div></div>","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":"23 5","pages":"Article e01069"},"PeriodicalIF":7.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148920160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Use of receptor and nonreceptor tyrosine kinase inhibitors and Parkinson disease risk","authors":"Giovanni R. Malaty,&nbsp;Jordan A. Killion,&nbsp;Sai Anmisha Doddamreddy,&nbsp;Osvaldo J. Laurido-Soto,&nbsp;Brad A. Racette","doi":"10.1016/j.neurot.2026.e01040","DOIUrl":"10.1016/j.neurot.2026.e01040","url":null,"abstract":"<div><div>There are currently no disease-modifying therapies for Parkinson disease (PD), although various targets for disease modification have been explored. Expression and binding of receptor tyrosine kinases (rTKs) and nonreceptor tyrosine kinases (nrTKs) have been implicated in PD pathogenesis, and their inhibition is a promisingneuroprotective strategy. This population-based, case-control study of US Medicare beneficiaries included 207,532 incident PD patients and 975,177 comparable, population-based control subjects from 2016 to 2018. This study investigated associations between Medicare Part D prescription fills prior to PD diagnosis for 7 rTK inhibitors (erlotinib, sorafenib, pazopanib, imatinib, sunitinib, nintedanib, and dasatinib) and 4 nrTK inhibitors (nilotinib, ibrutinib, ruxolitinib, and tofacitinib) and PD risk. Logistic regression estimated relative risks (RR) and 95% confidence intervals (CIs) adjusted for age, sex, race, smoking, and healthcare utilization. All medications were inversely associated with incident PD. The rTK inhibitors erlotinib (RR = 0.53, 95% CI: 0.38–0.74), sorafenib (RR = 0.43, 95% CI: 0.25–0.74), imatinib (RR = 0.60, 95% CI: 0.47–0.75), pazopanib (RR = 0.58, 95% CI: 0.39–0.86), nintedanib (RR = 0.66, 95% CI: 0.50–0.88), sunitinib (RR = 0.60, 95% CI: 0.39–0.93), and dasatinib (RR = 0.53, 95% CI: 0.35–0.82) had the strongest inverse associations. Among nrTK inhibitors, ibrutinib (RR = 0.62, 95% CI: 0.51–0.75) had a marked inverse association. Given the chemotherapeutic mechanisms of these medications, and the known cancer–PD inverse relationship, we performed a sensitivity analysis adjusting for relevant cancer subtypes, yielding a similar inverse association. Overall, the use of rTK and nrTK inhibitors was associated with a lower risk of developing PD, although there may be differential impact of this medication class depending on specific inhibition pathways.</div></div>","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":"23 5","pages":"Article e01040"},"PeriodicalIF":7.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148840778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Emerging Frontier of Neuromodulation for Delirium","authors":"Shixie Jiang","doi":"10.1016/j.neurot.2026.e01057","DOIUrl":"10.1016/j.neurot.2026.e01057","url":null,"abstract":"","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":"23 5","pages":"Article e01057"},"PeriodicalIF":7.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148875071","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}