Approaches for the induction of neurogenesis and neuronal recovery through several modalities are gaining popularity in Parkinson\'s disease (PD). Growth hormone (GH) seems to have a role in the reversal of neural function following brain injury as well as in normal brain development and function; therefore, the use of GH may represent a feasible strategy in the management of PD. This experimental study aimed to evaluate the effect of growth hormone on motor function and dendrite morphology in rats with 6-hydroxydopamine (6-OHDA)-induced PD model. Thirty-six Sprague Dawley rats were included and randomly allocated into one of the six study groups: two controls and four treatment groups that received daily subcutaneous growth hormone injections for 21 days, 1, 2, and 3 months. PD model was induced through unilateral 6-OHDA injection to the nigrostriatal pathway. The following assessments were made: apomorphine rotation test, stepping test, and tissue examinations for tyrosine hydroxylase and dendrite morphology. The apomorphine rotation test and the stepping test confirmed the presence of PD. These tests as well as dendritic spine density/number and length assessments showed improvement in PD findings over time with GH administration. Findings of this study suggest that GH administration may improve dendrite morphology and motor function in the PD model, which may translate into symptom relief and quality of life improvement in patients with PD. Such potential benefits should be tested in robust clinical studies.

In intracerebral hemorrhage (ICH), the mechanical brain injury is a considerable and indispensable factor determining the neurological functions and poor outcomes. Previous studies indicate the mechanically gated ion channel-Piezo1 can transduce mechanical effects following ICH. Isoquercitrin (ISQ) is a well-studied ion channel inhibitor. Furthermore, whether the following Piezo1-mediated neurological impairment can be ameliorated by ISQ remains unclear. Herein, we constructed the hydrostatic pressure model and ICH rat model. Firstly, we found that Piezo1 agonists Yoda1 and Jedi1 facilitated extracellular calcium influx dramatically, but ISQ could depress intracellular Ca2+ overload under hydrostatic pressure in primary neurons. Then we detected the expression profile of Piezo1, NLRP3 and NF-κB p-p65 after ICH, and found that the expression of Piezo1 was much earlier than NLRP3 and NF-κB p-p65. Furthermore, by western blot and immunofluorescence, ISQ decreased the expression of Piezo1 and NLRP3 dramatically like GsMTx4, but Nigericin as a NLRP3 agonist failed to affect Piezo1. Besides, both ISQ and interfering Piezo1 suppressed the upregulated caspase-1, NF-κB p-p65, p-IκBα, Tunel-positive cells and inflammatory factors (IL-1β, IL-6 and TNF-α) in ICH. At last, the hydrostatic pressure or hematoma induced disturbed neural viability, disordered neural cytomorphology, and increased neurobehavioral and cognitive deficits, but they were improved by ISQ and GsMTx4 strongly. Therefore, ISQ could alleviate neurological injuries induced by Piezo1 via NLRP3 pathway. These observations indicated that Piezos might be the new therapeutic targets, and blocking Piezos/NLRP3 pathway by ISQ could be an auspicious strategy for the treatment of ICH.

A proportion of patients infected with severe acute respiratory syndrome coronavirus 2 experience a range of neuropsychiatric symptoms months after infection, including cognitive deficits, depression and anxiety. The mechanisms underpinning such symptoms remain elusive. Recent research has demonstrated that nervous system injury can occur during COVID-19. Whether ongoing neural injury in the months after COVID-19 accounts for the ongoing or emergent neuropsychiatric symptoms is unclear. Within a large prospective cohort study of adult survivors who were hospitalized for severe acute respiratory syndrome coronavirus 2 infection, we analysed plasma markers of nervous system injury and astrocytic activation, measured 6 months post-infection: neurofilament light, glial fibrillary acidic protein and total tau protein. We assessed whether these markers were associated with the severity of the acute COVID-19 illness and with post-acute neuropsychiatric symptoms (as measured by the Patient Health Questionnaire for depression, the General Anxiety Disorder assessment for anxiety, the Montreal Cognitive Assessment for objective cognitive deficit and the cognitive items of the Patient Symptom Questionnaire for subjective cognitive deficit) at 6 months and 1 year post-hospital discharge from COVID-19. No robust associations were found between markers of nervous system injury and severity of acute COVID-19 (except for an association of small effect size between duration of admission and neurofilament light) nor with post-acute neuropsychiatric symptoms. These results suggest that ongoing neuropsychiatric symptoms are not due to ongoing neural injury.

Understanding the chemical events following trauma to the central nervous system could assist in identifying causative mechanisms and potential interventions to protect neural tissue. Here, we apply a partial optic nerve transection model of injury in rats and use synchrotron X-ray fluorescence microscopy (XFM) to perform elemental mapping of metals (K, Ca, Fe, Cu, Zn) and other related elements (P, S, Cl) in white matter tracts. The partial optic nerve injury model and spatial precision of microscopy allow us to obtain previously unattained resolution in mapping elemental changes in response to a primary injury and subsequent secondary effects. We observed significant elevation of Cu levels at multiple time points following the injury, both at the primary injury site and in neural tissue near the injury site vulnerable to secondary damage, as well as significant changes in Cl, K, P, S, and Ca. Our results suggest widespread metal dyshomeostasis in response to central nervous system trauma and that altered Cu homeostasis may be a specific secondary event in response to white matter injury. The findings highlight metal homeostasis as a potential point of intervention in limiting damage following nervous system injury.

Propofol, a commonly used intravenous anesthetic, has been associated with neurodegeneration in the developing brain upon repeated exposure. Dexmedetomidine is an α2 adrenoceptor agonist that was previously reported to possess neuroprotective properties. Here, we confirmed the impacts of dexmedetomidine on propofol-induced neuroapoptosis and subsequent spatial learning and memory deficits in neonatal rats. We found that dexmedetomidine effectively mitigated propofol-induced spatial learning and memory impairments and improved aversive memory in developing rats. Dexmedetomidine reduced propofol-induced cell apoptosis in the hippocampus and modulated the mRNA expression of Bcl-2 and Bax. Additionally, dexmedetomidine attenuated the propofol-induced increase of inflammatory factors IL-6 and TNF-α. The reduced phosphorylation levels of Akt and CREB levels by propofol were re-activated by dexmedetomidine. In conclusion, our findings demonstrated that dexmedetomidine effectively mitigated propofol-induced cognitive and memory impairments in developing rats by modulating apoptosis and reducing inflammation via activating the Akt/CREB/BDNF signaling pathway. These findings suggest potential strategies to protect the developing brain from the adverse effects of anesthetics and improve patient care in pediatric anesthesia practice.

UNASSIGNED: To explore the effects of customized 3D-printed assistive technology (AT) on functional performance and feasibility in patients with neurological impairment.
UNASSIGNED: Patients with neurological impairment were recruited and randomized into customized 3D-printed assistive device group (group 1; n = 17) or standard device group (group 2; n = 14). The device was designed to assist their writing, spoon using, and typing. Each patient underwent 4-week intervention with the device (30 min per session, twice a week).
UNASSIGNED: We observed significant differences in shoulder abduction (p = .00), external rotation (p = .01), and internal rotation (p = .02) in group 1. And significant differences in abduction (p = .05) and external rotation (p = .05) between the 2 groups. Group 1 achieved significant improvements in writing without AT (p = .04) and with AT (p = .02), spoon use without AT (p = .02) and with AT (p = .03), and hemiplegia-side typing with AT (p = .00). Group 2 achieved significant improvements in writing without AT (p = .01), hemiplegia-side typing without AT (p = .01), and bil-side typing with AT (P = .05). Moreover, no significant differences were noted in other outcome measures.
UNASSIGNED: This study demonstrated that customized 3D-printed AT can improve shoulder active motion for patients with neurological impairment. A positive effect in functional hand tasks after AT intervention. Offering customized AT with specific training could enhance the efficacy of interventions. The feasibility of using 3D printing technology to produce customized AT, which has the potential to be cost-effective and efficient.
3D-printed assistive device incorporating a splint can improve shoulder active motion compared to conventional assistive device for patients with neurological impairment.A positive effect in functional hand tasks after assistive device intervention.

Given the complexity of care necessitated after an acute traumatic spinal cord injury (SCI), it seems intuitively beneficial for such care to be delivered at hospitals with specialized SCI expertise. Demonstrating these benefits is not straightforward, however. We sought to determine whether specialized acute hospital care influenced the most fundamental outcomes after SCI: mortality within the first year of injury. We compared survival among patients with incomplete tSCI admitted to a single quaternary-level trauma hospital with a specialized acute SCI program versus those admitted to trauma hospitals without specialized acute SCI care. We performed a population-based retrospective observational cohort study using administrative and clinical data linked from multiple sources in British Columbia (BC) from 2001 to 2017. Among a cohort of 1920 patients, there were 193 deaths within one year. We failed to identify a significant overall benefit for survival after adjusting for potential confounders, and the confidence intervals (CIs) were compatible with both benefit and harm (odds ratio [OR] 1.01, 95% CI 0.17 to 6.11, p = 0.99). Significant associations were observed with age greater than 65 (OR 4.92, 95% CI 1.66 to 14.57, p < 0.01), Charlson Comorbidity Index (OR 1.61, 95% CI 1.42 to 1.83, p < 0.01), Injury Severity Score (OR 1.08, 95% CI 1.06 to 1.11, p < 0.01), and traumatic brain injury (OR 2.12, 95% CI 1.32 to 3.41, p < 0.01). Among patients with acute tSCI, admission to a hospital with specialized acute SCI care was not associated with improved overall one-year survival. Subgroup analyses, however, suggested heterogeneity of effects, with little benefit for older patients with less polytrauma and substantial benefit for younger patients with greater polytrauma.

Background: Traditional Chinese medicines exhibit promising preventive effects on Alzheimer\'s disease. Chaihu Shugan San (CSS) is a well-known traditional herbal formula whose several kinds of ingredients have the potential of ameliorating Alzheimer\'s disease. The present study aimed to evaluate the effects of CSS on the microbiota-gut-brain axis and cognitive deficits of senescence-accelerated mouse prone 8 (SAMP8) mice as well as investigate the underlying mechanisms. Methods: Thirty 5-month-old SAMP8 mice were randomly divided into the model group (SAMP8), CSS low-dose treatment group (CSSL), and CSS high-dose treatment group (CSSH). Ten SAMR1 mice were used as the normal control, and ten SAMP8 mice treated with donepezil were used as the positive control of cognitive function. CSS was orally administrated to SAMP8 mice for 8 weeks. The Morris water maze test was used to evaluate cognitive function. Histological staining was used to observe neuronal injury and Aβ deposition. Transmission electron microscopy was used to observe the synaptic ultrastructure. 16S rRNA gene analysis was performed to measure the changes in intestinal microbiota. Results: The results showed that CSS significantly improved the learning function and memory deficits of aged SAMP8 mice in the Morris water maze examination. CSS ameliorated neuronal injury, synaptic injuries, and Aβ deposition in the brain of SAMP8 mice. In addition, CSS also significantly improved microbiota composition in terms of elevating Lactobacillus reuteri and decreasing Staphylococcus xylosus in the feces of aged SAMP8 mice. Conclusion: These findings suggested that CSS might have a preventive potential for cognitive deficits in aging through regulating gut microbiota, which paved the way for the application of CSS for prevention and therapeutic purposes for mild cognitive impairment as well as Alzheimer\'s disease.

UNASSIGNED: Neurofilament light chain protein (NfL) is a fluid biomarker of neural injury measurable in cerebrospinal fluid and blood. Patients with different neurodegenerative disorders and mild traumatic brain injury display elevated levels of NfL. However, so far, elevated levels of NfL have not been demonstrated in persons with psychiatric disorders. To our knowledge, the occurrence of NfL in the blood has not previously been studied in persons undergoing forensic psychiatric assessment or persons treated in forensic mental health services. Supposedly, these persons suffer from experiences and conditions with a higher risk of neural injury than other psychiatric patients.
UNASSIGNED: In this pilot study, we investigated plasma levels of NfL in 20 persons undergoing forensic psychiatric assessment and 20 patients at a forensic psychiatric hospital. NfL values were compared with control groups of healthy individuals matched for age and sex.
UNASSIGNED: The prevalence of increased NfL in both forensic groups was low and did not differ compared with the controls. However, some persons undergoing forensic psychiatric assessment showed slightly elevated values.
UNASSIGNED: The slightly elevated values were observed in the group investigated closer in time to the index crime, when elevated NfL levels could be expected to be more prevalent due to acute conditions from the time of the offense. This gives reason to look further into this group.

Alzheimer\'s disease (AD) is one of the leading causes of death throughout the world. Z-DNA binding protein 1 (ZBP1), a DNA-related gene, is associated with inflammation, and its expression is altered in AD brain. We aimed to elucidate the exact role of ZBP1 in AD development and its potential regulatory mechanism. First, we constructed both in vivo and in vitro models of AD and investigated the ZBP1 expression profile. A loss-of-function assay was performed by transfecting lentivirus carrying ZBP1 short hairpin RNA (shRNA). By evaluating cell death, oxidative stress, inflammation response and pyroptosis, the function of ZBP1 was validated. Finally, the correlation between ZBP1 and interferon regulatory factor 3 (IRF3) was verified. We also performed rescue experiments to validate the crucial role of IRF3 in ZBP1-mediated AD progression. According to our results, ZBP1 was upregulated in AD rat tissue and AD neurons. Silencing ZBP1 dramatically decreased cell injury, oxidative stress and inflammation in AD neurons and improved the cognitive function of AD rats. Additionally, IRF3 expression and phosphorylation were significantly elevated during AD development and positively correlated with ZBP1. Taken together, silencing ZBP1 suppressed cell injury and pyroptosis of AD neurons and improved cognitive function of AD rats via inhibiting IRF3. These findings might provide a novel insight for AD target diagnosis and therapy.