Journal of neurotrauma最新文献

{"title":"<i>Response to Letter:</i> \"A Brock String Procedure Is Not Comprehensive Optometric Vision Therapy\".","authors":"Alicia M Trbovich, Aaron J Zynda, Anne Mucha, Anthony Kontos","doi":"10.1177/08977151261497218","DOIUrl":"https://doi.org/10.1177/08977151261497218","url":null,"abstract":"","PeriodicalId":16512,"journal":{"name":"Journal of neurotrauma","volume":" ","pages":"8977151261497218"},"PeriodicalIF":3.8,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149127827","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression of Concern.","authors":"","doi":"10.1177/08977151251364787","DOIUrl":"10.1177/08977151251364787","url":null,"abstract":"","PeriodicalId":16512,"journal":{"name":"Journal of neurotrauma","volume":" ","pages":"NP8"},"PeriodicalIF":3.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mild Traumatic Brain Injury Alters Hippocampal Sharp-Wave Ripple Properties: Implications in Memory Impairments.","authors":"Brian Noble, Ryota Homma, John I Broussard, Dustin Robinson, Anthony N Moore, Pramod K Dash","doi":"10.1177/08977151261434221","DOIUrl":"10.1177/08977151261434221","url":null,"abstract":"<p><p>A large body of evidence has shown that sharp wave ripples (SWRs), highly synchronized oscillations of the local field potential (LFP) in the CA1 pyramidal layer of the hippocampus, play a prominent role in memory consolidation. SWRs typically occur in periods of non-REM sleep, but have also been observed during awake rest periods of animals engaged in cognitive tasks. These events have been observed in rodents, non-human primates, and humans, suggesting they are evolutionarily conserved and contribute to memory formation. Numerous neurological diseases and insults, including traumatic brain injury (TBI), impair learning and memory. Mild TBI (mTBI) is the most prevalent form of TBI, and can cause memory impairments that, in some cases, last for months-to-years. Clinical and experimental studies have shown that these impairments can occur in the absence of visible physical damage to the hippocampus. In the present study, we examined whether an mTBI alters the properties of SWRs in rodents. Seven days after a mild fluid percussion injury (mFPI), recording electrodes were implanted into the CA1 subfield of the hippocampus of sham and injured rats. After seven days of recovery, LFPs and the activity of CA1 neurons were simultaneously recorded. Recordings were carried out when animals were exploring an arena containing two objects, one of which was moved between recording sessions. This allowed us to evaluate how changes in the environment affected SWR incidence and properties. Our data show that compared to uninjured controls, mFPI rats had reduced numbers of SWR events. Of the SWRs recorded, those from mTBI rats had shorter durations, reduced power, and higher frequencies than those in control animals. We also found that the modulation of the activity of CA1 pyramidal neurons by SWRs was markedly impaired in mTBI animals. Taken together, our data indicate that mTBI alters the electrophysiological properties of SWRs and reduces the synchronization of pyramidal neuron activity to SWRs. These electrophysiological changes may have implications in mTBI-associated memory impairments.</p>","PeriodicalId":16512,"journal":{"name":"Journal of neurotrauma","volume":" ","pages":"1670-1680"},"PeriodicalIF":3.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147473964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preconditioning Effect of Hydrogen Gas on Traumatic Brain Injury.","authors":"Masaya Nakagawa, Satoshi Tomura, Terushige Toyooka, Kazuya Fujii, Arata Tomiyama, Kojiro Wada","doi":"10.1177/08977151261432145","DOIUrl":"10.1177/08977151261432145","url":null,"abstract":"<p><p>Traumatic brain injury (TBI) affects approximately 1% of the global population annually. In Japan, sports-related head injuries are recognized as one of the most common causes. There have been reports suggesting that TBI sustained during sports activities may become more severe because of the added oxidative stress compared with injuries at rest, but there are still few reports on the actual changes in oxidative stress following TBI. Therefore, we first examined the changes in oxidative stress immediately post-sports-related TBI. No pharmacological treatment has been established to effectively prevent TBI, and preconditioning approaches aimed at enhancing endogenous tolerance prior to injury have attracted attention. However, existing methods often involve invasive procedures, limiting their clinical applicability. Prior studies demonstrated the therapeutic potential of hydrogen gas, which possesses antioxidant properties in TBI. Therefore, we examined whether hydrogen administration prior to TBI could attenuate secondary brain injury in a model incorporating exercise-induced oxidative stress before trauma. Male C57BL/6 mice (6 weeks old) were subjected to treadmill exercise at 15 m/min for 90 min to induce oxidative stress. During exercise, 1.3% hydrogen gas was delivered into the chamber for preconditioning. Moderate TBI was induced using a controlled cortical impact (CCI) device immediately postexercise. Four groups were evaluated: resting controls, exercise alone, exercise followed by TBI induced by CCI (ExCCI), and hydrogen-preconditioned exercise followed by TBI. Oxidative stress was assessed using hippocampal malondialdehyde (MDA) levels, and antioxidant capacity was evaluated using manganese superoxide dismutase (MnSOD) activity. Brain edema was quantified using brain water content, and vasogenic edema was assessed using Evans Blue extravasation. Histological analysis of the pericontusional cortex included glial fibrillary acidic protein (GFAP) and aquaporin-4 (AQP4) immunofluorescence. MDA levels increased 3 h postexercise and remained elevated for 24 h when TBI was induced. Hydrogen preconditioning significantly reduced MDA levels and enhanced MnSOD activity, which peaked 24 h postinjury. At the same time point, ExCCI mice showed significant brain and vasogenic edema, both of which were attenuated by hydrogen. GFAP and AQP4 were increased in ExCCI mice and suppressed by hydrogen. Although hydrogen is known to disappear from the blood within approximately 1 h postinhalation, MnSOD activity remained elevated for up to 24 h postinjury, indicating endogenous antioxidant defense activation. Hydrogen is considered to mitigate blood-brain barrier vulnerability to oxidative stress, thereby reducing vasogenic edema. These findings indicate that hydrogen gas may be effective as a treatment and a preventive intervention for TBI.</p>","PeriodicalId":16512,"journal":{"name":"Journal of neurotrauma","volume":" ","pages":"1636-1652"},"PeriodicalIF":3.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147512829","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Subconcussive Preconditioning Modifies Acute Microglial Response and Improves Cognitive Outcomes Post-Concussion.","authors":"Erin D Anderson, Kyulee Kim, Anastasia P Georges, Annika Naveen, Elena Grajales, Daunel V Augustin, David F Meaney","doi":"10.1177/08977151261433816","DOIUrl":"10.1177/08977151261433816","url":null,"abstract":"<p><p>Subconcussive impacts are highly prevalent in contact sports and are thought to increase concussion risk. However, the specific conditions under which these subconcussive impacts influence concussion outcomes are uncertain, limiting our understanding of the mechanisms behind repetitive head trauma. Given that subconcussive impacts elicit a microglial response, we examined how subconcussive preconditioning affects microglial morphology and transcriptomic profile, as well as cognitive outcome after concussion. To investigate this question, we developed and validated a scalable, closed-head controlled cortical impact model. Using this approach, we found that although concussion elicited morphological features of hyper-surveillant microglia at 1 day post-injury, they resolved by 9 days post-injury, and subconcussive impacts only produced microglial changes at 9 days post-injury. When subconcussive impacts preceded a concussive impact (i.e., preconditioned concussion), no changes in microglial morphology appeared at either 1 day or 9 days after injury. Subconcussive preconditioning also upregulated microglial genes associated with inhibiting pro-inflammatory pathways and enhancing folate metabolism. Interestingly, subconcussive preconditioning eliminated concussion-associated cognitive deficits in novel object recognition and this cognitive protection was time dependent: preconditioning impacts were only protective if delivered within 2 min of concussion and had no effect if delivered over a 48-h window. These results suggest that some types of subconcussive impacts may offer protection against subsequent concussion and mitigate changes in microglial morphology and inflammatory responses. Understanding this timing window could inform strategies for minimizing cognitive impairments in athletes exposed to repetitive head trauma.</p>","PeriodicalId":16512,"journal":{"name":"Journal of neurotrauma","volume":" ","pages":"1653-1669"},"PeriodicalIF":3.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147512884","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurotrauma During Military Training: Results of the INVestigating traIning assoCiated blasT pAthology (INVICTA) Study.","authors":"Michael J Roy, David O Keyser, Marcia Dovel, Rie Leverett, Alexander Hill, Kenneth Andres Manlapaz, Christopher K Rhea, Joshua T Lawton, Thaddeus Haight, Chen Lai, Devon Kulinski, Douglas S Brungart, Grant D Tays, Walter S Carr","doi":"10.1177/08977151261488794","DOIUrl":"https://doi.org/10.1177/08977151261488794","url":null,"abstract":"<p><p>Concern is growing that subconcussive blast exposure during military exercises such as heavy weapons training (HWT) may adversely affect brain function. HWT involves firing shoulder-mounted weapons that can expose the gunner, assistant gunner, and instructors (range safety officers [RSOs]) to blast overpressure >4.0 psi. Every HWT participant sustains repeated blast exposure: gunner and assistant alternate firing within an event, and instructors supervise multiple firings at approximately 12 HWTs over two years. This five-year study was designed to quantify blast exposure and serially assess a broad array of brain function measures in HWT participants and corresponding controls. Two hundred and twenty-four participants were prospectively assessed: 104 exposed special operators (SOs) firing live rounds in HWT; 47 SOs completing land warfare training without firing live rounds during HWT (training controls); 36 conventional active duty controls (ADCs); and 37 instructors. Assessments were conducted at baseline and at 30 min, 6, 24, and 72 h, 2 weeks, and 3 months post-HWT. Instructors were also assessed 9 and 18 months after their first HWT, with repeat of all acute assessments (30 min through 3 months) after their 18-month HWT. Blast exposure was measured with the Black Box Biometrics Generation 7 Blast Gauge System. Assessments included blood biomarkers, symptom scales, memory, cerebrovascular reactivity, electroencephalography (EEG), oculomotor function, gait, tactile discrimination, and hearing acuity. SOs exhibited significant alterations in short-term memory, complexity of electroencephalographic signals, and the blood biomarkers tau and ubiquitin C-terminal hydrolase L1 within minutes after HWT, while gait and oculomotor function were measurably altered within hours. More than 20% of the exposed had at least one significant change in a hearing threshold on audiologic assessment, though this, as well as changes in levels of the blood biomarker neurofilament-light, were observed two weeks after HWT. Instructors who experienced repeated HWT exposure over two-year duty tours demonstrated greater magnitude and duration alterations in memory and gait toward the end of those tours. The blood biomarker glial fibrillary acidic protein, vasomotor reactivity of the middle cerebral arteries, and seven cognitive tests comprising the Automated Neuropsychological Assessment Metrics Version 4 showed no significant changes in association with subconcussive blast exposure in this setting. Blast exposure during HWT is associated with acute changes in some blood biomarker levels and measures of brain function such as short term recall memory and gait. The effects appear to be short in duration, but recovery may be delayed after repeated exposure.</p>","PeriodicalId":16512,"journal":{"name":"Journal of neurotrauma","volume":" ","pages":"8977151261488794"},"PeriodicalIF":3.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149111007","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurorepair in Spinal Cord Injury: Convergent MicroRNA-Mediated Pathways Drive Astrocyte Pathology and Their Relevance to Human Biomarker Development.","authors":"Mehek Sharma, Hedong Li","doi":"10.1177/08977151261498691","DOIUrl":"10.1177/08977151261498691","url":null,"abstract":"<p><p>Spinal cord injury (SCI) initiates a complex secondary injury cascade characterized by neuroinflammation, astrocyte reactivity, neuronal loss, and glial scar formation, all of which influence endogenous repair and functional recovery. Emerging evidence identifies microRNAs (miRNAs) as post-transcriptional regulators of these processes, yet their integrated role in astrocyte-associated pathology and their translational relevance remain incompletely defined. Experimental studies indicate that miRNAs can modulate conserved signaling pathways, including NF-κB, MAPK, PI3K/AKT/mTOR, and JAK/STAT, with reported effects on astrocyte reactivity, inflammatory responses, neuronal survival, axonal regeneration, and blood-spinal cord barrier (BSCB) integrity. Additionally, miRNAs have been implicated in epigenetic regulation and mitochondrial function, which may influence glial proliferation and scar formation. In parallel, human studies of acute SCI demonstrate dynamic, severity-associated changes in circulating and cerebrospinal fluid miRNA profiles. Some of these human miRNA signatures overlap with inflammatory, apoptotic, and metabolic pathways identified in experimental models, although the biological sources and functional significance of these circulating signals remain incompletely defined. Human data remain largely descriptive and have not yet been fully integrated with mechanistic insights from preclinical astrocyte-focused studies. This review consolidates preclinical and human evidence to define a pathway-level framework in which miRNAs may contribute to astrocyte-associated pathology, glial scar dynamics, and neurorepair after SCI. By relating experimentally defined miRNA mechanisms to human biofluid signatures, miRNA networks represent potential translational targets for biomarker development and future therapeutic investigation. This framework provides a rationale for further evaluation of miRNA-based strategies in traumatic SCI, with potential future relevance to SCI occurring in the setting of spinal surgery.</p>","PeriodicalId":16512,"journal":{"name":"Journal of neurotrauma","volume":" ","pages":"8977151261498691"},"PeriodicalIF":3.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149194542","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Wearable Tracking of Eye and Body Movements During Breaching Training: Toward Real-Time Blast Injury Monitoring.","authors":"Jeremy P Kemmerer, James R Williamson, Joseph Kim, Elizabeth Halford, Hrishikesh M Rao, Christopher J Smalt","doi":"10.1177/08977151261433837","DOIUrl":"10.1177/08977151261433837","url":null,"abstract":"<p><p>Repeated exposure to blast overpressure in occupational settings has been associated with changes in cognitive and psychological health, as well as deficits in neurosensory subsystems. In this work, we describe a wearable system to simultaneously monitor physiology and blast exposure levels and demonstrate how this system can identify individualized exposure levels corresponding to acute physiological response to blast exposure. Machine learning was used to develop a dose-response model that fused multiple physiological measures (electrooculuography, gait, and balance) into a single risk score by predicting the level of blast exposure on held-out subjects (Fused model, <i>R</i> = 0.60). For our system, cohort, and environment, we found that blast events with peak pressure levels as low as 0.3 pound per square inch (PSI) could be related to physiological changes with blast exposure. We also identified an individual subject with longitudinally increasing reaction time scores who consistently showed a rapid and anomalous change in physiology-based risk scores after exposure to low-level blast events. Our results suggest that wearable technology may be viable for measuring physiological changes that are related to occupational blast exposure. Ultimately, this approach might be used to prevent neurotrauma from repeated exposure and to help set limits for a population or on an individual basis.</p>","PeriodicalId":16512,"journal":{"name":"Journal of neurotrauma","volume":" ","pages":"1623-1635"},"PeriodicalIF":3.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147512950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MEG Working Memory N-Back Task Revealed Functional Deficits in Children with Mild Traumatic Brain Injury.","authors":"Ming-Xiong Huang, Annemarie Angeles-Quinto, Ashley Robb-Swan, Erin D Bigler, Elisabeth A Wilde, Florin Vaida, Emily A Troyer, John R Hesselink, Chung-Kuan Cheng, Wenjing Meng, Elise Zimmerman, Jeffrey E Max","doi":"10.1177/08977151261433776","DOIUrl":"10.1177/08977151261433776","url":null,"abstract":"<p><p>Mild traumatic brain injury (mTBI) is a leading cause of sustained cognitive complaints in children. However, the TBI-related mechanisms underlying persistent cognitive symptoms including working memory (WM) dysfunction are not fully understood. Few pediatric studies of WM deficits in mTBI have taken advantage of the temporal and frequency resolution afforded by electromagnetic measurements. Using magnetoencephalography (MEG) and an N-back WM task, we investigated functional abnormalities in children with mTBI within a 3-week post-injury period. Children aged 8-15 years with mTBI (<i>n</i> = 60) and orthopedic injury (OI) controls (<i>n</i> = 37) from consecutive admissions to an emergency department were studied prospectively. MEG source-magnitude images were obtained for alpha (8-12 Hz), beta (15-30 Hz), gamma (30-90 Hz), theta (4-7 Hz), and delta (1-4 Hz) frequency bands. Compared with OI controls, children with mTBI showed decreased MEG signals (hypoactivity) across frequency bands in the proper WM network including dorsolateral prefrontal cortex (dlPFC), anterior cingulate cortex, and supramarginal gyrus (SMG), but over-recruitment with increased MEG signals (hyperactivity) in the frontal pole and ventromedial prefrontal cortex. The MEG activity from dlPFC and SMG regions also correlated with changes in symptom scores between 3-week and 3-month behavioral exams. This is the first pediatric study showing MEG hypoactivity from the WM proper network and over recruitment outside the WM network. One mechanism that may explain these novel findings could be the gamma-aminobutyric acid (GABA)-ergic inhibitory interneuron injury, which may cause disinhibition in the WM neural network, directly eliminating synchronized signals that are normally evoked by stimuli. This MEG study of abnormal MEG responses evoked by WM N-back stimuli provides a new functional imaging marker for pediatric mTBI.</p>","PeriodicalId":16512,"journal":{"name":"Journal of neurotrauma","volume":" ","pages":"1569-1582"},"PeriodicalIF":3.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147948583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interferon-β Deficiency Selectively Modulates Chronic Microglial Pathways after Traumatic Brain Injury.","authors":"James P Barrett, Rebecca J Henry, Maria Vaida, Kari Ann Shirey, Stefanie N Vogel, Alan I Faden, Bogdan A Stoica","doi":"10.1177/08977151261434894","DOIUrl":"10.1177/08977151261434894","url":null,"abstract":"<p><p>Traumatic brain injury (TBI) induces long-term, secondary injury processes that contribute to chronic neurodegeneration and associated neurological deficits. Previously, we demonstrated that controlled cortical impact in mice, a well-established experimental model of TBI, causes acute neuroinflammatory changes, including upregulation of interferon-β (IFN-β) and other type I interferon (IFN-I)-related genes in the injured cortex and hippocampus. Early inhibition of IFN-β signaling, either through intracerebroventricular administration of an anti-type I IFN receptor antibody or use of global IFN-β knockout mice (IFN-β^-/-), attenuates post-traumatic neuroinflammation and neurodegeneration and improves neurological outcomes for up to 28 days postinjury (dpi), with the knockout model showing more robust and sustained protective effects. However, the consequences of sustained suppression of these pathways after TBI have not been studied. Here, we examine the long-term effects of IFN-β deficiency on microglial activation, neuropathology, and neurological function during the chronic phase post-TBI (60-90 dpi). Transcriptomic analysis of isolated microglia from wild-type mice after TBI revealed persistent upregulation of IFN-I and other key neuroinflammatory genes, including classical pro-inflammatory and disease-associated microglia (DAM) at both 60 and 90 dpi. The IFN-I pathway was significantly attenuated in IFN-β^-/- mice at these later timepoints. However, IFN-β deficiency did not significantly alter the trauma-induced upregulation of DAM markers, indicating selectivity of chronic IFN-β modulation on injury-induced microglia-reactive phenotypes. Moreover, although IFN-β deficiency significantly attenuated pro-inflammatory phenotypes at 60 dpi, it enhanced the injury-mediated downregulation of homeostatic microglial genes at 90 dpi. In addition, no significant reduction in lesion volume or fine motor deficits was observed in IFN-β^-/- mice at chronic timepoints, although chronic post-traumatic cognitive impairment was attenuated. These findings suggest that global IFN-β deficiency has complex, time-dependent effects on chronic outcomes following TBI; although it improves cognitive function, it further suppresses homeostatic microglia that may partially limit long-term therapeutic benefits.</p>","PeriodicalId":16512,"journal":{"name":"Journal of neurotrauma","volume":" ","pages":"1681-1699"},"PeriodicalIF":3.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147581543","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}