Neurobiochemical Changes Research Articles

Effects of quercetin-immobilized albumin cerium oxide nanoparticles on glutamate toxicity: in vitro study.

One aspect of glutamate (Glut) toxicity may be the opening of the blood-brain barrier to albumin (Al), which in itself can cause nerve cell death. Quercetin (Q) is a polyphenolic substance and has a neuroprotective effect. Cerium oxide nanoparticles (Ce2O3NPs) are highly interested in biological applications due to their antioxidant properties. The current study aimed to investigate the impact of Q-immobilized Al+Ce2O3NPs in Glut-induced neurotoxicity, mainly focusing on cell viability and neurobiochemical changes. Hydrothermal synthesis and characterization of Q-immobilized Al+Ce2O3NPs were performed. After preparing the primary neuron culture, it was exposed to Glut to induce neurotoxicity. Then, various doses of Ce2O3NP, Al+Ce2O3NP, and Q+Al+Ce2O3NPs (1, 5, 10, and 25 µg/ml) were applied to the wells and incubated for 24 h. Then, cell viability was determined by MTT analysis. Additionally, oxidative stress parameters were measured. When the obtained data were examined, it was shown that cell viability decreased with Glut concentration but significantly increased with Q+Al+Ce2O3NPs treatment. When oxidative stress markers were considered, Glut treatment increased LDH, AChE, and TOS levels, while TAC and GSH levels decreased. However, the trend changed after Q+Al+Ce2O3NPs treatment, suggesting that damaged neurons were protected against oxidative stress. The results of this study indicate that Q+Al+Ce2O3NP can ameliorate Glut-induced neurotoxicity, especially when used at a dose of 25 µg/ml.

Correction: Acute neuro-biochemical changes induced by nitrogen-tungsten co-doped titanium dioxide nanoparticles

Correction: Acute neuro-biochemical changes induced by nitrogen-tungsten co-doped titanium dioxide nanoparticles

Acute neuro-biochemical changes induced by nitrogen-tungsten co-doped titanium dioxide nanoparticles

Nitrogen-tungsten co-doped titanium dioxide nanoparticles (W-N-doped TiO2 NPs) are employed for the photocatalytic degradation of environmental pollutants. However, the potential impact of these nanoparticles on the central nervous system remains a subject of concern. This study aimed to evaluate the effects of W-N-doped TiO2 NPs on neurophysiological and biochemical parameters of healthy rat brains, including behavioral monitoring, electroencephalogram analysis, and oxidative stress markers quantification. Intraperitoneal administration of W-N-doped TiO2 NPs to rats revealed abnormal brain electrical activity and an altered sense of balance in the treated rats. The ability of W-N-doped TiO2 NPs to cross the blood–brain barrier and accumulate in the brain leads to oxidative stress damage, supported by the elevated levels of reactive oxygen species (ROS), nitrite concentration, and malondialdehyde levels. Additionally, exposure to W-N-doped TiO2 NPs significantly reduced the antioxidant enzyme levels, such as catalase and superoxide dismutase, impacting a significant decrease in dopamine and acetylcholinesterase within the rat neural tissue. Furthermore, the inflammatory biomarker tumor necrosis factor-alpha and 8-hydroxy 2-deoxyguanosine significantly increased in response to W-N-doped TiO2 NPs. The findings revealed the adverse effects of W-N-doped TiO2 NPs on the electrical activity of rat brains and the altered concentration of various neuro-biomarkers, highlighting their potential neurotoxicity.

The Neuropathological Impacts of COVID-19: Challenges and Alternative Treatment Options for Alzheimer's Like Brain Changes on Severely SARS-CoV-2 Infected Patients.

Recently, some researchers claimed neuropathological changes lead to Alzheimer's-like brains after severe infection of SARS-CoV-2. Several mechanisms have been postulated on how SARS-CoV-2 neurological damage leads to Alzheimer's disease (AD) development. Neurobiochemical changes during infection may significantly induce Alzheimer's disease in severely COVID-19 infected people. The immune system is also compromised while infected by this novel coronavirus. However, recent studies are insufficient to conclude the relationship between Alzheimer's disease and COVID-19. This review demonstrates the possible pathways of neuropathological changes induced by the SARS-CoV-2 virus in AD patients or leading to AD in COVID-19 patients. Therefore, this study delineates the challenges for COVID-19 infected AD patients and the mechanism of actions of natural compounds and alternative treatments to overcome those. Furthermore, animal studies and a large cohort of COVID-19 survivors who showed neuroinflammation and neurological changes may augment the research to discover the relationship between Alzheimer's disease and COVID-19.

Synthetic azo-dye, Tartrazine induces neurodevelopmental toxicity via mitochondria-mediated apoptosis in zebrafish embryos

Tartrazine (TZ), or E 102 or C Yellow, is a commonly used azo dye in the food and dyeing industries. Its excessive usage beyond permissible levels threatens human health and the aquatic environment. While previous studies have reported adverse effects such as mutagenicity, carcinogenicity, and reproductive toxicity. Our study aimed to comprehensively evaluate the developmental neurotoxicity of TZ exposure via biochemical and behavioral examinations and explored the underlying mechanism via gene expression analyses. TZ at an environmentally relevant concentration (50 mg/L) significantly induces oxidative stress, altered antioxidant (SOD, CAT and GSH) response, triggered cellular damage (MDA and LDH), and induced neuro-biochemical changes (AChE and NO). Gene expression analyses revealed broad disruptions in genes associated with antioxidant defense (sod1, cat, and gstp1), mitochondrial dysfunction (mfn2, opa1, and fis1),evoked inflammatory response (nfkb, tnfa, and il1b), apoptosis activation (bcl2, bax, and p53), and neural development (bdnf, mbp, and syn2a). Behavioral analysis indicated altered thigmotaxis, touch response, and locomotion depending on the concentration of TZ exposure. Remarkably, the observed effective concentrations were consistent with the permitted levels in food products, highlighting the neurodevelopmental effects of TZ at environmentally relevant concentrations. These findings provide valuable insights into the underlying molecular mechanisms, particularly the role of mitochondria-mediated apoptosis, contributing to TZ-induced neurodevelopmental disorders in vivo.

Normalization of HPA Axis, Cholinergic Neurotransmission, and Inhibiting Brain Oxidative and Inflammatory Dynamics Are Associated with The Adaptogenic-like Effect of Rutin Against Psychosocial Defeat Stress.

Social defeat stress (SDS) due to changes in biochemical functions has been implicated in the pathogenesis of affective and cognitive disorders. Employing pharmacological approach with adaptogens in the management and treatment of psychosocial stress is increasingly receiving scientific attention. In this study, we investigated the neuroprotective effect of rutin, a bioflavonoid with neuroprotective and anti-inflammatory functions on neurobehavioral and neuro-biochemical changes in mice exposed to SDS. Groups of mice named the intruder mice received normal saline(10 mL/kg), rutin (5, 10, and 20mg/kg, i.p.), and ginseng (50mg/kg, i.p.) daily for 14days, and then followed by 10min daily SDS (physical/psychological) exposures to aggressor micefrom days 7-14. Investigations consisting of neurobehavioral (locomotion, memory, anxiety, and depression)phenotypes, neuro-biochemical (oxidative, nitrergic, cholinergic, and pro-inflammatory cytokines) levelsin discrete brain regions, and hypothalamic-pituitary-adrenal(HPA) axis consistingadrenalweight, corticosterone, and glucoseconcentrations were assessed. Rutin restored the neurobehavioral deficits and reduced the activity of acetylcholinesterase in the brains. Adrenal hypertrophy, increased serum glucose and corticosterone levels were significantly attenuated by rutin. SDS-induced release of tumor necrosis factor-alpha and interleukin-6 in the striatum, prefrontal cortex, and hippocampus were also suppressed by rutin in a brain-region-dependent manner. Moreover, SDS-induced oxidative stress characterized by low antioxidants (glutathione, superoxide-dismutase, catalase) and lipid peroxidation and nitrergic stress were reversed by rutin in discrete brain regions. Collectively, our data suggest that rutin possesses an adoptogenic potential in mice exposed to SDS via normalization of HPA, oxidative/nitrergic, and neuroinflammatory inhibitions. Thus, may be adopted in the management of neuropsychiatric syndrome due to psychosocial stress.

Biological, physiological, neurobiological, neurophysiological pathogenesis of Alzheimer’s, dementia, neurodegenerative diseases:

AbstractBackgroundHuman beings use all sensory organs in biological/physiological, neurological/functional ways to feed the brain/brain cells with necessary input/impulses of all environment information for the brain. Practical review: Our lifestyle, ‐losing anymore in life emotional our reactions are: fear, stress, panic, aggressive, depressive, affected person withdraws him/herself: forgets daily life structures/real‐world, loses relationships of any kind , falls backwards in development stages.Methoda)physiological system: In body/brain are changes of pathological biochemical/neuobiochemical milieu. The brain cells will not work through less neurotransmitters, the brain cells go down.‐The pathological milieu in brain is through less input functions of sensory organs, without/less consciousness.Resulta)Factual review results are:‐cognitive/perceptions skills dysfunctions,‐abilities wakefulness is less,‐deficiencies/shortcomings disorders, ‐reality misconceptions, ‐daily life relationship loss,‐brain related disorders: ‐"vascular earlier microcirculatory failure in brain, Damage of Brain Cells”, ‐neurodegenerative diseases,‐and metabolisms disorders through: ‐ our lifestyle, ‐unhealthy nutrition, ‐not enough fluid intake,‐occupying all sensory organs. b)physiological system: It’s ‐too little fluid, too little blood speed, ‐oxygen lack, ‐nutrients distribution, detoxification, exchanges in cells are too slow. This leads to slower metabolism. ‐And delay processing of motor output with, –movement/balance disorders, ‐brain cells metabolic disturbances,‐circulatory disorders, ‐focus/concentration difficulties.‐perceptions disorders,‐ incorrectly feelings/movements. Through poor flow blood properties: ‐blood speed reduction, ‐brain circulatory disorders,‐body/brain oxygen lack, ‐harmful toxins and medication reactions can not be controlled in combination mix with alcohol. All calling up:‐pathological/neurobiochemical reactions in the brain and this leads to neurodegenerative diseases. ‐c)practical systemresults‐abilities wakefulness/perceptions of all sensory organs are less.‐ deficiencies/shortcomings disorders, ‐reality misconceptions, ‐relationship loss to daily‐life. System: Molecular in brain: a)‐through neurobiochemical changes, neurotransmitters building themselves are low, leads to brain cells death. b)‐synapses transmissions glutamate failures, molecular reactions are misfolded proteins productions, with pathological neurobiochemical reactions: growth of fibrils, amyloids, blockades other brain cells. Cells death : power of weight, press, speed of brain cell death. Human being is dead. It's a normal wrongful process.ConclusionIn practical work:‐prevent, stop this, ‐follow biological, physiological function to feed your human brain/brain cells. Therapy is “Rediscover Recovery Practical Reference Training”, multidisciplinary work fields. The goal is: affected person status rebuilding, person’s reintegration in family (not as patient),

Neurobehavioral and neurobiochemical changes in arsenic treated male mice

Arsenic is an element that raises much concern from the both environmental and human health. The effects of As on learning behavior, neurotransmitters, and oxidative stress indicators were studied in male Swiss white mice. The purpose of this study was to explore into the preliminary work described concerning memory, biochemical changes, and learning impairment in mice exposed to arsenic. The study results in the Shuttle box, Water-maze, T-Maze tests and body weight measurements, As-treated males demonstrated decreased body weight and learning behavior. Dopamine, DA, serotonin, 5-HA, and cholinesterase, AchE levels were all decreased. When compared to the control, GSH and the enzymes GST, CAT, and SOD activity were decreased, while TBARS was raised. This study concludes as the essential reasons that explain the causes of As influence on learning and other data, based on the results collected and other previous studies in this field. In general, additional research is required to determine As negative effects on various elements of human and animal health.

Minority Stress and the Effects on Emotion Processing in Transgender Men and Cisgender People: A Study Combining fMRI and 1H-MRS.

BackgroundMinority stress via discrimination, stigmatization, and exposure to violence can lead to development of mood and anxiety disorders and underlying neurobiochemical changes. To date, the neural and neurochemical correlates of emotion processing in transgender people (and their interaction) are unknown.MethodsThis study combined functional magnetic resonance imaging and magnetic resonance spectroscopy to uncover the effects of anxiety and perceived stress on the neural and neurochemical substrates, specifically choline, on emotion processing in transgender men. Thirty transgender men (TM), 30 cisgender men, and 35 cisgender women passively viewed angry, neutral, happy, and surprised faces in the functional magnetic resonance imaging scanner, underwent a magnetic resonance spectroscopy scan, and filled out mood- and anxiety-related questionnaires.ResultsAs predicted, choline levels modulated the relationship between anxiety and stress symptoms and the neural response to angry and surprised (but not happy faces) in the amygdala. This was the case only for TM but not cisgender comparisons. More generally, neural responses in the left amygdala, left middle frontal gyrus, and medial frontal gyrus to emotional faces in TM resembled that of cisgender women.ConclusionsThese results provide first evidence, to our knowledge, of a critical interaction between levels of analysis and that choline may influence neural processing of emotion in individuals prone to minority stress.

Neuroprotective Potentials of Cocculus hirsutus Leaf Extract Against 6,7-Epoxytropine Tropate-Induced Memory Impairment in Rats

Cocculus hirsutus, a tropical South Asian creeper,traditionally used as a diuretic, laxative, cardiotonic, anti-microbial, antidiabetic, anti-inflammatory and spermatogenic. However, the neuroprotective role was less explored; therefore, this researchwas conducted to investigate neuroprotective potentials of Cocculus hirsutus leaf hydroalcoholic extract in 6,7-Epoxytropine tropate (Scopolamine) induced cognitive impairment and oxidative lipid peroxidation in the brain of wistar albino rat. Scopolamine (1 mg/kg body weight, i.p.) was given in rats for 14 days to induce transient cognitive impairment. Donepezil (2 mg/kg body weight, orally) has been used for this research as a positive control. Behavioral studies were done using Morris water maze and elevated plus maze and neurobiochemical parameters such as acetylcholinesterase activity, reduced glutathione levels and activity of catalase were assessed in rats brain homogenate. Cocculus hirsutus leaf hydroalcoholic extract(200 mg/kg and 400 mg/kg) exhibited an improvement in spatial, exteroceptive learning and memory. The extract showed significant decline in the activity of acetylcholinesterase, enhancement of reduced glutathione levels and catalase activity (p<0.001). All the outcomes were assessed by Bonferroni post hoc tests with ANOVA for multiple comparison studies. This study reveals that hydroalcoholic extract of Cocculus hirsutusleaf acts as neuroprotective against scopolamine induced behavioral and neurobiochemical changes.

Crosstalk of hypothalamic chemerin, histamine, and AMPK in diet-and olanzapine-induced obesity in rats

AimContradiction overwhelms chemerin link to feeding behavior. Neither the chemerin central role on appetite regulation nor its relation to hypothalamic histamine and AMPK is verified. Main methodsFood intake, body weight and hypothalamic biochemical changes were assessed after a single intra-cerebroventricular or intraperitoneal injection (ip) (1 μg/kg or 16 μg/kg, respectively) or chronic ip administration (8 μg/kg/day) of chemerin for 14 or 28 days. Hypothalamic neurobiochemical changes in chemerin/histamine/AMPK induced by either 8-week high fat diet (HFD) or food restriction were also investigated. To confirm chemerin-histamine crosstalk, these neurobiochemical changes were assessed under settings of H1-receptor agonism and/or antagonism by betahistine and/or olanzapine, respectively for 3 weeks. Key findingsChemerin-injected rats exhibited anorexigenic behavior in both acute and chronic studies that was associated with a decreased AMPK activity in the arcuate nucleus (ARC). However, with long-term administration, chemerin anorexigenic effect gradually ceased. Contrarily to food restriction, 8-week HFD increased ARC expression of chemerin and its receptor CMKLR1, reducing food intake via an interplay of H1-receptors and AMPK activity. Blockage of H1-receptors by olanzapine disrupted chemerin signaling pathway with an increased AMPK activity, augmenting food intake. These changes were reversed to normal by betahistine coadministration. SignificanceChemerin is an anorexigenic adipokine, whose dysregulation is implicated in diet, and olanzapine-induced obesity through a histamine/AMPK axis in the ARC. Hypothalamic chemerin/CMKLR1 expression is a dynamic time-dependent response to changes in body weight and/or food intake. Targeting chemerin as a novel therapeutic approach against antipsychotic- or diet-induced obesity is worth to be further delineated.

Concordance of Immune-Related Markers in Lymphocytes and Prefrontal Cortex in Schizophrenia.

Schizophrenia is a severe neuropsychiatric disorder associated with a wide array of transcriptomic and neurobiochemical changes. Genome-wide transcriptomic profiling conducted in postmortem brain have provided novel insights into the pathophysiology of this disorder, and identified biological processes including immune/inflammatory-related responses, metabolic, endocrine, and synaptic function. However, few studies have investigated whether similar changes are present in peripheral tissue. Here, we used RNA-sequencing to characterize transcriptomic profiles of lymphocytes in 18 nonpsychotic controls and 19 individuals with schizophrenia. We identified 2819 differentially expressed transcripts (Pnominal < .05) in the schizophrenia group when compared to controls. Bioinformatic analyses conducted on a subset of 293 genes (Pnominal < .01 and |log2 FC| > 0.5) highlighted immune/inflammatory responses as key biological processes in our dataset. Differentially expressed genes in lymphocytes were highly enriched in gene expression profiles associated with cortex layer 5a and immune cells. Thus, we investigated whether the changes in transcripts levels observed in lymphocytes could also be detected in the prefrontal cortex (PFC, BA10) in a second replication cohort of schizophrenia subjects. Remarkably, mRNA levels detected in the PFC and lymphocytes were in strong agreement, and measurements obtained using RNA-sequencing positively correlated with data obtained by reverse transcriptase-quantitative polymerase chain reaction analysis. Collectively, our work supports a role for immune dysfunction in the pathogenesis of schizophrenia and suggests that peripheral markers can be used as accessible surrogates to investigate putative central nervous system disruptions.

Neuro-biochemical changes induced by zinc oxide nanoparticles.

Nanoparticles are now widely used in various aspects of life, especially zinc oxide nanoparticles (ZnNPs) that used in mouth washing, cosmetics, sunscreens, toothpaste and root canal flings. This research aims to determine the impact of ZnNPs on healthy mice's brain tissue. ZnNPs have caused major changes in the brain monoamines (dopamine, norepinephrine and serotonin) and ions such as Ca2+, Na+, K+ and Zn2+. Concerning the histological picture, administration of ZnNPs caused some histopathological impairment in brain tissue. In addition, ZnNPs reduced the level of glutathione and catalase in brain tissue, although an increase in the level of nitrite / nitrate and ROS was observed, while the level of malondialdhyde was not significantly altered. Moreover, ZnNPs induced DNA fragmentation in brain of mice. Collectively, the obtained results revealed that ZnNPs affected the brain levels of investigated monamines, ions, enzymatic and non-enzymatic antioxidants thus they may have potential influence on central nervous system.

Dietary Total Prenylflavonoids from the Fruits of Psoralea corylifolia L. Prevents Age-Related Cognitive Deficits and Down-Regulates Alzheimer's Markers in SAMP8 Mice.

Alzheimer’s disease (AD) is a serious threat for the aging society. In this study, we examined the preventive effect of the total prenylflavonoids (TPFB) prepared from the dried fruits of Psoralea corylifolia L., using an age-related AD mouse model SAMP8. We found that long-term dietary TPFB at 50 mg/kg·day significantly improved cognitive performance of the SAMP8 mice in Morris water maze tests, similar to 150 mg/kg·day of resveratrol, a popular neuro-protective compound. Furthermore, TPFB treatment showed significant improvements in various AD markers in SAMP8 brains, which were restored to near control levels of the normal mice, SAMR1. TPFB significantly reduced the level of amyloid β-peptide 42 (Aβ42), inhibited hyperphosphorylation of the microtubule-associated protein Tau, induced phosphorylation of Ser9 of the glycogen synthase kinase 3β (GSK-3β), and decreased the expression of the proinflammatory cytokines TNFα, IL-6, and IL-1β. Finally, TPFB also markedly reduced the level of serum derivatives of reactive oxygen metabolites (d-ROMs), a biomarker of oxidative stress in vivo. These results showed that dietary TPFB could effectively prevent age-related cognitive deficits and AD-like neurobiochemical changes, and may have a potential role in the prevention of Alzheimer’s disease.

Combined brain Fe, Cu, Zn and neurometabolite analysis - a new methodology for unraveling the efficacy of transcranial direct current stimulation (tDCS) in appetite control.

Obesity is a chronic, multifactorial origin disease that has recently become one of the most frequent lifestyle disorders. Unfortunately, current obesity treatments seem to be ineffective. At present, transcranial direct current brain stimulation (tDCS) represents a promising novel treatment methodology that seems to be efficient, well-tolerated and safe for a patient. Unfortunately, the biochemical action of tDCS remains unknown, which prevents its widespread use in the clinical arena, although neurobiochemical changes in brain signaling and metal metabolism are frequently reported. Therefore, our research aimed at exploring the biochemical response to tDCS in situ, in the brain areas triggering feeding behavior in obese animals. The objective was to propose a novel neurochemical (serotoninergic and dopaminergic signaling) and trace metal analysis of Fe, Cu and Zn. In doing so, we used energy-dispersive X-ray fluorescence (EDXRF) and high-performance liquid chromatography (HPLC). Anodal-type stimulation (atDCS) of the right frontal cortex was utilized to down-regulate food intake and body weight gain in obese rats. EDXRF was coupled with the external standard method in order to quantify the chemical elements within appetite-triggering brain areas. Major dopamine metabolites were assessed in the brains, based on the HPLC assay utilizing the external standard assay. Our study confirms that elemental analysis by EDXRF and brain metabolite assay by HPLC can be considered as a useful tool for the in situ investigation of the interplay between neurochemical and Fe/Cu/Zn metabolism in the brain upon atDCS. With this methodology, an increase in both Cu and Zn in the satiety center of the stimulated group could be reported. In turn, the most significant neurochemical changes involved dopaminergic and serotoninergic signaling in the brain reward system.

Changes in gene expression and sensitivity of cocaine reward produced by a continuous fat diet.

Preclinical studies report that free access to a high-fat diet (HFD) alters the response to psychostimulants. The aim of the present study was to examine how HFD exposure during adolescence modifies cocaine effects. Gene expression of CB1 and mu-opioid receptors (MOr) in the nucleus accumbens (N Acc) and prefrontal cortex (PFC) and ghrelin receptor (GHSR) in the ventral tegmental area (VTA) were assessed. Mice were allowed continuous access to fat from PND 29, and the locomotor (10mg/kg) and reinforcing effects of cocaine (1 and 6mg/kg) on conditioned place preference (CPP) were evaluated on PND 69. Another group of mice was exposed to a standard diet until the day of post-conditioning, on which free access to the HFD began. HFD induced an increase of MOr gene expression in the N Acc, but decreased CB1 receptor in the N Acc and PFC. After fat withdrawal, the reduction of CB1 receptor in the N Acc was maintained. Gene expression of GHSR in the VTA decreased during the HFD and increased after withdrawal. Following fat discontinuation, mice exhibited increased anxiety, augmented locomotor response to cocaine, and developed CPP for 1mg/kg cocaine. HFD reduced the number of sessions required to extinguish the preference and decreased sensitivity to drug priming-induced reinstatement. Our results suggest that consumption of a HFD during adolescence induces neurobiochemical changes that increased sensitivity to cocaine when fat is withdrawn, acting as an alternative reward.

HIV-associated neurodegeneration and neuroimmunity: multivoxel MR spectroscopy study in drug-naïve and treated patients.

The aim of this study was to test neurobiochemical changes in normal appearing brain tissue in HIV+ patients receiving and not receiving combined antiretroviral therapy (cART) and healthy controls, using multivoxel MR spectroscopy (mvMRS). We performed long- and short-echo 3D mvMRS in 110 neuroasymptomatic subjects (32 HIV+ subjects on cART, 28 HIV+ therapy-naïve subjects and 50 healthy controls) on a 3T MR scanner, targeting frontal and parietal supracallosal subcortical and deep white matter and cingulate gyrus (NAA/Cr, Cho/Cr and mI/Cr ratios were analysed). The statistical value was set at p < 0.05. Considering differences between HIV-infected and healthy subjects, there was a significant decrease in the NAA/Cr ratio in HIV+ subjects in all observed locations, an increase in mI/Cr levels in the anterior cingulate gyrus (ACG), and no significant differences in Cho/Cr ratios, except in ACG, where the increase showed trending towards significance in HIV+ patients. There were no significant differences between HIV+ patients on and without cART in all three ratios. Neuronal loss and dysfunction affects the whole brain volume in HIV-infected patients. Unfortunately, cART appears to be ineffective in halting accelerated neurodegenerative process induced by HIV but is partially effective in preventing glial proliferation. • This is the first multivoxel human brain 3T MRS study in HIV. • All observed areas of the brain are affected by neurodegenerative process. • Cingulate gyrus and subcortical white matter are most vulnerable to HIV-induced neurodegeneration. • cART is effective in control of inflammation but ineffective in preventing neurodegeneration.

Neurobiochemical changes in the vicinity of a nanostructured neural implant.

Neural interface technologies including recording and stimulation electrodes are currently in the early phase of clinical trials aiming to help patients with spinal cord injuries, degenerative disorders, strokes interrupting descending motor pathways, or limb amputations. Their lifetime is of key importance; however, it is limited by the foreign body response of the tissue causing the loss of neurons and a reactive astrogliosis around the implant surface. Improving the biocompatibility of implant surfaces, especially promoting neuronal attachment and regeneration is therefore essential. In our work, bioactive properties of implanted black polySi nanostructured surfaces (520–800 nm long nanopillars with a diameter of 150–200 nm) were investigated and compared to microstructured Si surfaces in eight-week-long in vivo experiments. Glial encapsulation and local neuronal cell loss were characterised using GFAP and NeuN immunostaining respectively, followed by systematic image analysis. Regarding the severity of gliosis, no significant difference was observed in the vicinity of the different implant surfaces, however, the number of surviving neurons close to the nanostructured surface was higher than that of the microstructured ones. Our results imply that the functionality of implanted microelectrodes covered by Si nanopillars may lead to improved long-term recordings.

Inflammatory insult during pregnancy accelerates age-related behavioral and neurobiochemical changes in CD-1 mice.

Data shows that inflammation during pregnancy significantly exerts a long-term influence on offspring, such as increasing the risk of adult cognition decline in animals. However, it is unclear whether gestational inflammation affects the neurobehavioral and neurobiochemical outcomes in the mother-self during aging. In this study, pregnant CD-1 mice intraperitoneally received lipopolysaccharide (LPS) in two doses (25 and 50g/kg, respectively) or normal saline daily during gestational days 15-17. At the age of 15months, a battery of behavioral tasks was employed to evaluate their species-typical behaviors, sensorimotor ability, anxiety levels, and spatial learning and memory abilities. An immunohistochemical method was utilized preliminarily to detect neurobiochemical indicators consisting of amyloid-β, phosphorylated tau, presynaptic proteins synaptotagmin-1 and syntaxin-1, glial fibrillary acidic protein (GFAP), and histone-4 acetylation on the K8 site (H4K8ac). The behavioral results showed that LPS exposure during pregnancy exacerbated a decline in 15-month-old CD-1 mice's abilities to nest, their sensorimotor and spatial learning and memory capabilities, and increased their anxiety levels. The neurobiochemical results indicated that gestational LPS exposure also intensified age-related hippocampal changes, including increased amyloid-β42, phosphorylated tau, synaptotagmin-1 and GFAP, and decreased syntaxin-1 and H4K8ac. Our results suggested that the inflammatory insult during pregnancy could be an important risk factor for the development of Alzheimer's disease, and the H4K8 acetylation might play an important role in the underlying mechanism. This study offers a perspective for improving strategies that support healthy development and successful aging.

Teismo psichiatrijos pacientų smurtinio elgesio rizikos veiksniai

Teismo psichiatrija – specifinė sritis, kurioje susipina teisiniai, klinikiniai ir socialiniai aspektai. Svarbu teisingai įvertinti ir apsaugoti abi puses: tiek visuomenę, tiek nepakaltinamais dėl psichikos sutrikimo pripažintus asmenis, siekiant jų resocializacijos. Tarp jų dažniausiai nustatomi psichikos sutrikimai yra psichoziniai, ypač šizofrenija, intelekto sutrikimas. Priklausomybė nuo psichoaktyvių medžiagų yra ir gretutinė lydinti liga, ir smurtinį elgesį provokuojantis veiksnys. Studijose išskiriama, kad reikia atkreipti dėmesį į asmenybės sutrikimus, asmenybines charakterio ypatybės, kadangi tai turi įtakos smurtinio elgesio prognozei. Nagrinėjant teismo psichiatrijos klausimus bene daugiausia dėmesio skiriama smurtinio elgesio rizikos veiksnių nustatymui, diagnostinių skalių kūrimui. Kaip biologiniai smurtinio elgesio rizikos veiksniai įvardijami neuroanatominiai, neurobiocheminiai pakitimai galvos smegenyse, kurie aptinkami atliekant pažangius neurovizualinius galvos smegenų tyrimus. Be to, neuromediatorių, hormonų koncentracijos pokyčiai, pacientų patirtos galvos traumos yra susiję su didesne jų smurto rizika.