Neurobehavioral Test Battery Research Articles

BMP Antagonist Gremlin 2 Regulates Hippocampal Neurogenesis and Is Associated with Seizure Susceptibility and Anxiety.

The Bone Morphogenetic Protein (BMP) signaling pathway is vital in neural progenitor cell proliferation, specification, and differentiation. The BMP signaling antagonist Gremlin 2 (Grem2) is the most potent natural inhibitor of BMP expressed in the adult brain; however its function remains unknown. To address this knowledge gap, we have analyzed mice lacking Grem2 via homologous recombination (Grem2-/- ). Histological analysis of brain sections revealed significant scattering of CA3 pyramidal cells within the dentate hilus in the hippocampus of Grem2-/- mice. Furthermore, the number of proliferating neural stem cells and neuroblasts was significantly decreased in the subgranular zone of Grem2-/- mice compared with that of wild-type (WT) controls. Due to the role of hippocampal neurogenesis in neurological disorders, we tested mice on a battery of neurobehavioral tests. Grem2-/- mice exhibited increased anxiety on the elevated zero maze in response to acute and chronic stress. Specifically, male Grem2-/- mice showed increased anxiogenesis following chronic stress, and this was correlated with higher levels of BMP signaling and decreased proliferation in the dentate gyrus. Additionally, when chemically challenged with kainic acid, Grem2-/- mice displayed a higher susceptibility to and increased severity of seizures compared with WTs. Together, our data indicate that Grem2 regulates BMP signaling and is vital in maintaining homeostasis in adult hippocampal neurogenesis and structure. Furthermore, the lack of Grem2 contributes to the development and progression of neurogenesis-related disorders such as anxiety and epilepsy.

A comparison of the social cognition and neurocognitive characteristics of adolescents with suicide behavior, adolescent with depression and healthy controls.

Deficits in neurocognition and social-cognition have been suggested to be an endophenotype for suicidal behavior. We aimed to compare the social-cognition and neurocognitive characteristics of adolescents diagnosed with depression with and without suicidal behavior and to investigate whether these functions predict suicide. Adolescents diagnosed with Major Depressive Disorder (MDD) with suicidal behavior (n = 42); MDD without suicidal behavior (n = 44) and age- and sex-matched controls (n = 43) were included. The University of Pennsylvania Computerized Neurobehavioral Test Battery and Autism Spectrum Screening Questionnaire (ASSQ) were used to evaluate social-cognition and neurocognitive characteristics. Several neurocognitive domain values of MDD groups, were significantly different from the control group. Neutral emotion recognition task (p = 0.025) and ASSQ scores were found to be significantly impaired in the patient groups (p < 0.001). Logistic regression analysis showed that, only the increase in the Suicide Probability Scale score was found to be significant as a risk factor predicting suicide (p = 0.007, OR: 1.246). While the neurocognitive and social-cognitive performances of adolescents with MDD were significantly lower than the control group, these performances in the two depression groups were similar. When the predictors of suicidal behavior were examined, it was found that only the increase in suicidal ideation scores predicted suicide.

The effect of magnesium sulfate on memory and anxiety-like behavior in a rat model: an investigation of its neuronal molecular mechanisms

ABSTRACT Background Anxiety is an adaptive response to potentially threatening conditions. Excessive and uncontrolled anxiety responses become nonadaptive and cause anxiety disorders. To better understand the anxiety-modulating effects of Mg sulfate, behavioral test batteries in the assessment of anxiety and learning and memory functions were performed simultaneously over a time period. This study also examines the effects of Mg sulfate compared to diazepam, an anxiolytic drug with amnestic effects on anxiety-like behavior, as well as possible oxidative-nitrosative stress and hippocampal changes in male rats exposed to predator odor. Methods Young adult Sprague-Dawley male rats were used. The rats were assessed using a comprehensive neurobehavioral test battery consisting of novel object recognition, open field, and successive alleys tasks. Anxiety was induced by cat odor, and diazepam and Mg were used as study drugs. Of the frontal cortex and hippocampus, the state of total oxidant and antioxidant and NO levels and histological examination of hippocampal CA1, CA2, CA3, and DG regions were performed. Results Diazepam- and Mg-treated rats showed an improvement in anxiety-related behavior to predator odors. Furthermore, Mg treatment alleviated some of the increasing oxidative stress in the frontal cortex and hippocampus of rats, while diazepam treatment in particular enhanced hippocampal oxidant and antioxidant activity. In addition, brain NO increase induced by animal odor exposure or diazepam treatment was ameliorated by Mg administration. Conclusions Overall, our work suggests that Mg had a partial anxiolytic effect on anxiety-like behaviors, although not as much as diazepam, and this effect varied depending on the dose. Mg treatment might counteract increased oxidative stress and elevated NO levels in the brain.

Sex-specific effects of alcohol on neurobehavioral performance and endoplasmic reticulum stress: an analysis using neuron-specific MANF deficient mice.

Excessive alcohol exposure can cause neurobehavioral deficits and structural alterations in the brain. Emerging research evidence suggests that endoplasmic reticulum (ER) stress plays an important role in alcohol-induced neurotoxicity. Mesencephalic astrocyte-derived neurotrophic factor (MANF) is an ER stress inducible protein and is responsible to maintain ER homeostasis. MANF is highly expressed in both the developing and mature brain. We have previously shown that MANF deficiency exacerbated alcohol induced neurodegeneration and ER stress in the developing brain. However, little is known regarding the role of MANF in alcohol induced neuronal damage in the adult brain. In this study, we used a neuron-specific MANF knockout (KO) mouse model to investigate the effect of MANF deficiency on acute binge alcohol exposure-induced neurobehavioral deficits and ER stress. Adult male and female MANF KO mice and littermate controls received daily alcohol gavage (5g/kg) for 10days and then subjected to a battery of neurobehavioral tests including rotarods, balance beam, DigiGait, open field, elevated plus maze, Barnes maze, and three-chamber sociability task. Female MANF KO animals were more susceptible to alcohol-induced body weight loss. Alcohol exposure did not affect motor function, however female but not male MANF KO mice exhibited an increased locomotor activity in open field test. Learning and memory was not significantly impaired, but it was altered by MANF deficiency in females while it was affected by alcohol treatment in males. Both alcohol-exposed male and female MANF KO mice displayed increased sociability. Alcohol induced the expression of ER chaperones GRP78 and GRP94 and altered the levels of several unfolded protein response (UPR) and neuroinflammation markers in MANF KO mice in a sex-specific manner. The expression of MANF interacting proteins neuroplastin, PDIA1, and PDIA6 was increased in MANF KO mice, and was further induced by alcohol. In conclusion, alcohol exposure and neuronal MANF deficiency interacted to alter neurobehavioral outcomes, ER homeostasis and neuroinflammation in a sex-specific manner.

Establishing a Measure of Educational Attainment: Using the Zambia Neurobehavioural Test Battery

Establishing a Measure of Educational Attainment: Using the Zambia Neurobehavioural Test Battery

Supplementation with vitamins D3 and a mitigates Parkinsonism in a haloperidol mice model

BackgroundEarlier reports suggest that vitamin D3 (Vit D3) supplementation attenuates Parkinsonism in drug-induced motor deficits. Moreover, the function of Vit D3 may be optimized by co-administration with vitamin A (Vit A). In line with the synergistic interplay between vitamins, we hypothesized that the efficacy of Vit D3 to attenuate Parkinsonism in a haloperidol-induced mouse model of motor deficits would be more potent when concomitantly administered with Vit A. MethodsThirty-six (36) adult male mice were randomly divided into six groups of six animals each: the control group, the PD model (haloperidol-treated only group) (-D2), and four other groups treated with haloperidol together with either one or two of the following vitamin supplementations: Vit D3, Vit A, Vit D3 +VA, or bromocriptine a known PD drug respectively. Motor functions were assessed using a battery of neurobehavioral tests in experimental animals, after which brain tissues were harvested and processed for biochemical and histomorphological analysis. ResultsWe recorded a significant decline in motor activity in the PD mice model treated with haloperidol alone compared to other experimental groups that received vitamin supplementations. The significant decrease in motor activity observed in the PD mice model corresponded with marked neurodegenerative features in the cytoarchitecture of the pyramidal cells in the striatum and primary motor cortex (M1). Furthermore, the haloperidol-induced PD mice model treated with Vit D3 +Vit A showed significant improvement in motor activity and attenuation of oxidative stress levels and neurodegenerative features compared to other groups treated with Vit A, Vit D3 and bromocriptine alone. ConclusionAltogether, our findings suggest that concomitant administration of both Vit D3 and Vit A prevents the development of Parkinsonism features in the haloperidol mouse model of motor deficit. Thus, supplementation with Vit D3 +Vit A may be a viable option for slowing the onset and progression of motor deficits.

Effects of short-term exposure to moderate pure carbon dioxide levels on cognitive performance, health symptoms and perceived indoor environment quality

Educational buildings frequently experience elevated CO2 concentrations with inadequate ventilation and high occupancy, sometimes exceeding building guideline levels. Some studies reported detrimental impacts on cognitive performance of indoor CO2 levels, while others did not. To generate further evidence, we conducted an experiment in an environmentally controlled chamber. Sixty-nine healthy university students were exposed individually for 70 min, in three separate sessions, to three CO2 conditions of 600, 1500 and 2100 ppm (crossover design). With fixed ventilation rates, pure CO2 was injected to achieve different exposure levels. A validated neurobehavioral BARS test battery was used to assess participants’ cognitive performance. Participants gave subjective ratings of indoor environment and reported any health symptom through questionnaires. Comparing elevated CO2 levels to 600 ppm, after adjusting for potential confounders, results showed significant improved performance, that is, responses were quicker in two out of ten tests, and no significant differences in accuracy for any test. Under 1500 ppm, participants rated the air quality significantly higher than at 600 ppm, but there were no differences at 2100 ppm. Differences were not significant on thermal sensation, perceived lighting quality, perceived noise level, or health symptoms for comparisons between conditions. Results indicate no clear link between pure CO2 levels below 2100 ppm and cognitive performance, perceived indoor environment quality and health symptoms. The findings are consistent with some prior studies, indicating that pure CO2 below 2100 ppm implies no harm in adults and should not be treated as a potential indoor pollutant in higher educational environments.

Influence of pesticide exposure on farmers' cognition: A systematic review.

Pesticide application has become necessary to increase crop productivity and reduce losses. However, the use of these products can produce toxic effects. Farmers are individuals occupationally exposed to pesticides, thus subject to associated diseases as well as cognitive impairment. However, this relation is not well established in the literature, requiring further investigation. To assess the potential association between farmers' pesticide exposure and cognitive impairment, we followed the preferred reporting items for systematic reviews and meta-analyses (PRISMA) guidelines, considering participants, interventions, comparators, outcomes, and study strategies. This study included articles published between 2000 and 2021 on the Scopus, Web of Science, ScienceDirect, and PubMed databases, retrieved by the terms "pesticides and cognition" and "pesticides and memory." In total, ten studies fit the established criteria and were included in the sample. All had farmers occupationally exposed to pesticides in their sample and only one study dispensed with a control group. Of the neurobehavioral tests, four studies used mini-mental state examination, six neurobehavioral core test batteries (tests recognized in the area), and the remaining, other tests. We observed that 90% of articles found an association between cognitive impairment and pesticide exposure. Overall, five studies measured the activity of cholinesterases in their sample, of which three found significant differences between groups, confirming intoxication in those exposed. Despite the limited number of trials, we found scientific evidence to support the existence of adverse effects of pesticides on farmers' cognition. We recommend that future studies research similar projects, expanding knowledge on the subject.

Intravitreal RTH258 (brolucizumab) demonstrates no effect on pregnancy, parturition, embryofetal or postnatal development in cynomolgus monkeys

RTH258 (brolucizumab) is a humanized single chain antibody fragment, the smallest functional unit of an antibody designed to target vascular endothelial growth factor in angiogenic retinal disease. To further understand the safe use of RTH258, this study assessed the potential impact of intravitreal RTH258 on pre- and postnatal development in the offspring of cynomolgus monkeys following administration to the mother. Three groups of 16 pregnant females were included: a low dose group (RTH258 3 mg/50 µl [60 mg/ml]), a high dose group (RTH258 6 mg/50 µl [120 mg/ml]), and a control group. Maternal animals were administered a single injection of 50 µl in the right eye once every four weeks. Animals were observed daily and detailed observations were collected before and after the first dose, and then weekly thereafter. Following parturition, observations of infants included external, morphological, and ophthalmic examinations; neurobehavioral test battery; grip strength; and skeletal development. Blood samples for hematology, coagulation, and clinical chemistry were collected from non-fasted maternal and infant animals. No RTH258-related deaths occurred in maternal dams or infants. No RTH258-related clinical observations were noted in maternal animals or in surviving infants - there were no changes in gestation length; pregnancy loss; deaths; body weight/weight change; infant grip strength; infant external, morphological, or skeletal evaluations; ophthalmoscopy or neurobehavioral observations; or clinical pathology parameters. RTH258 had no impact on pregnancy or parturition; embryo-fetal development; or survival, growth, or postnatal development of offspring when administered via repeated intravitreal administration.

Interleukin-4 mitigates anxiety-like behavior and loss of neurons and fiber tracts in limbic structures in a microglial PPARγ-dependent manner after traumatic brain injury

Traumatic brain injury (TBI) is commonly followed by intractable psychiatric disorders and long-term changes in affect, such as anxiety. The present study sought to investigate the effect of repetitive intranasal delivery of interleukin-4 (IL-4) nanoparticles on affective symptoms after TBI in mice. Adult male C57BL/6 J mice (10–12 weeks of age) were subjected to controlled cortical impact (CCI) and assessed by a battery of neurobehavioral tests up to 35 days after CCI. Neuron numbers were counted in multiple limbic structures, and the integrity of limbic white matter tracts was evaluated using ex vivo diffusion tensor imaging (DTI). As STAT6 is a critical mediator of IL-4-specific transcriptional activation, STAT6 knockout mice were used to explore the role of endogenous IL-4/STAT6 signaling axis in TBI-induced affective disorders. We also employed microglia/macrophage (Mi/Mϕ)-specific PPARγ conditional knockout (mKO) mice to test if Mi/Mϕ PPARγ critically contributes to IL-4-afforded beneficial effects. We observed anxiety-like behaviors up to 35 days after CCI, and these measures were exacerbated in STAT6 KO mice but mitigated by repetitive IL-4 delivery. We discovered that IL-4 protected against neuronal loss in limbic structures, such as the hippocampus and the amygdala, and improved the structural integrity of fiber tracts connecting the hippocampus and amygdala. We also observed that IL-4 boosted a beneficial Mi/Mϕ phenotype (CD206+/Arginase 1+/PPARγ+ triple-positive) in the subacute injury phase, and that the numbers of Mi/Mϕ appositions with neurons were robustly correlated with long-term behavioral performances. Remarkably, PPARγ-mKO completely abolished IL-4-afforded protection. Thus, CCI induces long-term anxiety-like behaviors in mice, but these changes in affect can be attenuated by transnasal IL-4 delivery. IL-4 prevents the long-term loss of neuronal somata and fiber tracts in key limbic structures, perhaps due to a shift in Mi/Mϕ phenotype. Exogenous IL-4 therefore holds promise for future clinical management of mood disturbances following TBI.

Effects of elevated carbon dioxide levels on response speed in cognitive test

To explore the associations of exposure to carbon dioxide with adults’ response speed, 69 participants were invited to participate in the experiment conducted in an environmentally controlled chamber. Participants were exposed alone in three separate sessions, each lasting one hour, with a fixed ventilation rate, temperature and relative humidity level and the CO2 levels fixed at 600ppm, 1500ppm and 2100ppm, respectively. A validated neurobehavioral test battery, the Behavioural Assessment and Research System (BARS) was used to assess participants’ cognitive performance, and response times were collected. Response speed was assessed in ten different tests. After adjusting for potential confounders (age, gender, and education), results showed no significant differences in eight out of the ten neurobehavioral tests. For the Selective Attention test, participants responded faster (lower response time) under CO2 levels of 2100ppm compared to 600ppm (adj.β-coef. -17.57, 95% CI (-29.45, -5.68), p-value=0.004). For the Progressive Ratio Test, participants’ response times significantly decreased with CO2 levels increased. Results indicate no statistical link between CO2 levels and response speed, with only two out of ten comparisons being significant.

Exposure to Organic Solvents and Neurobehavioral Assessment of Working Children of Informal Footwear Units of Agra, India.

Children aged 5 to 14 years are employed in the informal units of footwear making and are exposed to a mixture of organic solvents present in the adhesives. Organic solvents are reported to be toxic to the neurobehavioral system. The present study was undertaken among the working children of informal footwear units of Agra to assess neurobehavioral functions using neurobehavioral tests. The study included 151 working children and 157 school children. We used the interview technique to collect the data regarding demographic, occupational, personal, and clinical characteristics using a pre-designed and pre-tested proforma. Each study participant was then subjected to a neurobehavioral test battery that included digit symbol test, finger dexterity, tweezer dexterity, vocabulary test, picture completion, and maze completion test. The mean age of working children was 10.8 ± 1.5 years and that of school children was 11.0 ± 1.5 years. Except for the vocabulary test scores, all other test scores were significantly lower among working children as compared with the school children. The study revealed that the working children in informal footwear making units are exposed to a mixture of chemicals that affect their neurobehavioral function as reflected by poor neurobehavioral test battery (NBT) scores.

Human mood and cognitive function after different extreme cold exposure

Mood and cognitive function can change after cold exposure. Recovering from extreme cold is important, especially for people who work outdoors. This study was conducted to investigate cognitive function in the recovery period after being exposed to different temperatures of cold environments. 12 subjects underwent different cold exposures at −5 °C, −10 °C, and −15 °C in a climate chamber. Cognitive function was measured with the Neurobehavioral Core Test Battery (NCTB) and Stroop color-word test after 40 min of recovery at a room of 24 °C. The results showed that 40 min of recovery after cold exposure could not eliminate the differences between different degrees of extremely cold exposure in the mood effects (confusion-bewilderment). A decrease in ambient temperature could reduce visual perception and memory functions. Manual dexterity decreased by 13.6% in −10 °C compared with that in 24 °C due to colder ambient temperatures. At different degrees of cold exposure, selective attention decreased significantly as the ambient temperature dropped. The results from this study could be used to better organize work and rest periods according to task characteristics and duration of cold exposure.

Association between pesticide exposure and neurobehavioral performance of agricultural workers: A cross-sectional study.

BackgroundPesticide exposure has affected humans’ health, especially those directly in contact with a pesticide like agricultural workers. Here, we sought to see a link between pesticide exposure and cognitive impairment among male agricultural workers.MethodsWe selected 18–60 years old 100 male agricultural workers who came for their health check‐up in the hospital's out‐patient department from August 2020 to May 2021. Standardized questionnaires (German Q18 questionnaire) and WHO Neurobehavioral Core Test Battery were used to examine the neurobehavioral performance of the individuals. The data were presented in a descriptive manner and statistically examined using the chi‐square test.ResultsThe male agricultural workers’ neurobehavioral performance was 46% normal and 54% abnormal. Headaches, impaired focus, short memory, weariness, palpitation, and numbness were the most prevalent neurobehavioral impairments. The chi‐square test revealed that spraying frequency (p =.010), personal protective equipment (PPE) use (p < .001), and smoking habits (p =.006) were all linked to neurobehavioral performance, while spraying duration (p =.804), working years (p =.234), pesticide types (p =.816), and spraying time (p =.867) were not linked to neurobehavioral performance.ConclusionWe found that pesticide exposure has a certain role on neurobehavioral performance in adult male agricultural workers as more people have been affected; however, a considerable number of confounding factors might have played a significant role in giving rise to such results. The government should be concerned about farmer's neurobehavioral performance and implement different approaches to minimize the use of pesticides so that agricultural workers can work without any mental health problems.

Subarachnoid Hemorrhage Induces Sub-acute and Early Chronic Impairment in Learning and Memory in Mice.

Subarachnoid hemorrhage (SAH) leads to significant long-term cognitive deficits, so-called the post-SAH syndrome. Existing neurological scales used to assess outcomes of SAH are focused on sensory-motor functions. To better evaluate short-term and chronic consequences of SAH, we explored and validated a battery of neurobehavioral tests to gauge the functional outcomes in mice after the circle of Willis perforation-induced SAH. The 18-point Garcia scale, applied up to 4days, detected impairment only at 24-h time point and showed no significant difference between the Sham and SAH group. A decrease in locomotion was detected at 4-days post-surgery in the open field test but recovered at 30days in Sham and SAH groups. However, an anxiety-like behavior undetected at 4days developed at 30days in SAH mice. At 4-days post-surgery, Y-maze revealed an impairment in working spatial memory in SAH mice, and dyadic social interactions showed a decrease in the sociability in SAH mice, which spent less time interacting with the stimulus mouse. At 30days after ictus, SAH mice displayed mild spatial learning and memory deficits in the Barnes maze as they committed significantly more errors and used more time to find the escape box but still were able to learn the task. We also observed cognitive dysfunction in the SAH mice in the novel object recognition test. Taken together, these data suggest dysfunction of the limbic system and hippocampus in particular. We suggest a battery of 5 basic behavioral tests allowing to detect neurocognitive deficits in a sub-acute and chronic phase following the SAH.

Cortisol and C-Reactive Protein Vary During Sleep Loss and Recovery but Are Not Markers of Neurobehavioral Resilience.

Cortisol and C-reactive protein (CRP) typically change during total sleep deprivation (TSD) and psychological stress; however, it remains unknown whether these biological markers can differentiate robust individual differences in neurobehavioral performance and self-rated sleepiness resulting from these stressors. Additionally, little is known about cortisol and CRP recovery after TSD. In our study, 32 healthy adults (ages 27–53; mean ± SD, 35.1 ± 7.1 years; 14 females) participated in a highly controlled 5-day experiment in the Human Exploration Research Analog (HERA), a high-fidelity National Aeronautics and Space Administration (NASA) space analog isolation facility, consisting of two baseline nights, 39 h TSD, and two recovery nights. Psychological stress was induced by a modified Trier Social Stress Test (TSST) on the afternoon of TSD. Salivary cortisol and plasma CRP were obtained at six time points, before (pre-study), during [baseline, the morning of TSD (TSD AM), the afternoon of TSD (TSD PM), and recovery], and after (post-study) the experiment. A neurobehavioral test battery, including measures of behavioral attention and cognitive throughput, and a self-report measure of sleepiness, was administered 11 times. Resilient and vulnerable groups were defined by a median split on the average TSD performance or sleepiness score. Low and high pre-study cortisol and CRP were defined by a median split on respective values at pre-study. Cortisol and CRP both changed significantly across the study, with cortisol, but not CRP, increasing during TSD. During recovery, cortisol levels did not return to pre-TSD levels, whereas CRP levels did not differ from baseline. When sex was added as a between-subject factor, the time × sex interaction was significant for cortisol. Resilient and vulnerable groups did not differ in cortisol and CRP, and low and high pre-study cortisol/CRP groups did not differ on performance tasks or self-reported sleepiness. Thus, both cortisol and CRP reliably changed in a normal, healthy population as a result of sleep loss; however, cortisol and CRP were not markers of neurobehavioral resilience to TSD and stress in this study.

Brain innate immune response via miRNA-TLR7 sensing in polymicrobial sepsis

Sepsis-associated encephalopathy (SAE) occurs in sepsis survivors and is associated with breakdown of the blood–brain barrier (BBB), brain inflammation, and neurological dysfunction. We have previously identified a group of extracellular microRNAs (ex-miRNAs), such as miR-146a-5p, that were upregulated in the plasma of septic mice and human, and capable of inducing potent pro-inflammatory cytokines and complements. Here, we established a clinically relevant mouse model of SAE and investigated the role of extracellular miRNAs and their sensor Toll-like receptor 7 (TLR7) in brain inflammation and neurological dysfunction. We observed BBB disruption and a profound neuroinflammatory responses in the brain for up to 14 days post-sepsis; these included increased pro-inflammatory cytokines production, microglial expansion, and peripheral leukocyte accumulation in the CNS. In a battery of neurobehavioral tests, septic mice displayed impairment of motor coordination and neurological function. Sepsis significantly increased plasma RNA and miRNA levels for up to 7 days, such as miR-146a-5p. Exogenously added miR-146a-5p induces innate immune responses in both cultured microglia/astrocytes and the intact brain via a TLR7-dependent manner. Moreover, mice genetically deficient of miR-146a showed reduced accumulation of monocytes and neutrophils in the brain compared to WT after sepsis. Finally, ablation of TLR7 in the TLR7-/- mice preserved BBB integrity, reduced microglial expansion and leukocyte accumulation, and attenuated GSK3β signaling in the brain, but did not improve neurobehavioral recovery following sepsis. Taken together, these data establish an important role of extracellular miRNA and TLR7 sensing in sepsis-induced brain inflammation.

Neurocognitive deficits among adult road traffic accident victims at the University Teaching Hospital, Lusaka, Zambia

Introduction: Road traffic accidents (RTAs) are of growing public health importance worldwide contributing significantly to the global disease burden thus public health experts worldwide concede that there is a global epidemic of RTAs. Exposure to RTAs may be associated with changes in brain functioning and cognitive performance. Objective: This study sought to contribute to the understanding of the neurocognitive deficits among adult victims of RTAs. Methodology: It is a cross-sectional study (descriptive in nature). Cognitive profiles of the affected participants were assessed by selected tests from the International Neurobehavioral test battery. The quality of life was assessed by application of the World Health Organisation Quality of Life (WHOQOL) questionnaire. The primary data obtained was analyzed using descriptive and inferential statistics using SPSS. Results: Twenty-seven (27) RTA victims out of Thirty (30) had executive functioning impairment with a Domain Deficit Score (DDS) of ≥ 0.5 and all the RTA victims in the study had speed of information processing impairment with a Domain Deficit Score (DDS) of ≥ 0.5. There was no significant statistical gender difference in neurocognitive functioning (Executive functioning F=0.85, P=0.36; Speed of information processing F=0.98, P=0.33). Compromised quality of life among adult victims of road traffic accidents was confirmed (P=0.005). Conclusion: This study shows an association between RTA and neurocognitive functioning in adult victims. Findings of this study show the presence of neuropsychological impairments in the two domains assessed (executive functioning and speed of information processing). The study indicates that RTA significantly compromises the quality of life.

Intranasal delivery of interleukin-4 attenuates chronic cognitive deficits via beneficial microglial responses in experimental traumatic brain injury

Traumatic brain injury (TBI) is commonly followed by long-term cognitive deficits that severely impact the quality of life in survivors. Recent studies suggest that microglial/macrophage (Mi/MΦ) polarization could have multidimensional impacts on post-TBI neurological outcomes. Here, we report that repetitive intranasal delivery of interleukin-4 (IL-4) nanoparticles for 4 weeks after controlled cortical impact improved hippocampus-dependent spatial and non-spatial cognitive functions in adult C57BL6 mice, as assessed by a battery of neurobehavioral tests for up to 5 weeks after TBI. IL-4-elicited enhancement of cognitive functions was associated with improvements in the integrity of the hippocampus at the functional (e.g., long-term potentiation) and structural levels (CA3 neuronal loss, diffusion tensor imaging of white matter tracts, etc.). Mechanistically, IL-4 increased the expression of PPARγ and arginase-1 within Mi/MΦ, thereby driving microglia toward a global inflammation-resolving phenotype. Notably, IL-4 failed to shift microglial phenotype after TBI in Mi/MΦ-specific PPARγ knockout (mKO) mice, indicating an obligatory role for PPARγ in IL-4-induced Mi/MΦ polarization. Accordingly, post-TBI treatment with IL-4 failed to improve hippocampal integrity or cognitive functions in PPARγ mKO mice. These results demonstrate that administration of exogenous IL-4 nanoparticles stimulates PPARγ-dependent beneficial Mi/MΦ responses, and improves hippocampal function after TBI.

The Effect of Noise on the Neurobehavioral Function of the Occupational Population and the Content of Catecholamines.

According to the decibel level of noise detection in the working environment, the research objects were divided into high noise group (more than 85 dB), low noise group (55 to 85 dB), and control group (less than 55 dB), the neurobehavioral core test battery (NCTB) was used to systematic tests all workers, radioimmunoassay was used to detect plasma catecholamine levels, and the relationship between noise intensities and the levels of plasma catecholamine was analyzed by canonical correlation. The result shows noise exposure will affect workers' neurological function and the influence of noise on neurobehavioral function may be related to the increase of the levels of norepinephrine and dopamine in the plasma and the inhibition of the synthesis of epinephrine of noise-exposed workers.