Earlier studies suggested that damage to the right hemisphere leads to cognitive impairment in spatial working memory, but recent studies show that the right hemisphere is not required for visual priming as evaluated on fragment completion or stem completion tasks with a single potential completion. The lack of specialized emotional processing in the Left Hemisphere may explain why the influences of Right Hemisphere presentation on memory for visual specificity conversed with emotion but not the effects of Left Hemisphere presentation on memory for comprehension information. According to the current study, the discrepancies were influenced by different retrieval tasks used. Specifically, the right hemisphere isn't required for visual priming as analyzed by fragment completion or stem completion tasks with a single possible completion. Damage to the right hemisphere, on the other hand, disrupts visual priming for word stems with multiple completions. This is a literature review that focuses on effect damage to the right hemisphere and its role in disruption of visual priming for word stems with multiple completions. In the absence of the anterior sections of the corpus callosum, visual working memory continues to remain unified. This indicates that visual working memory is not housed in the frontal cortex and/or is not unified via direct callosal connections between the frontal cortices.

The identification of genes that are expressed differentially in the diseased versus healthy individual give relevant information regarding the pathology of the disease. The identification of DEGs can be a significant step in the field of clinical and pharmaceutical research. They can act as a potent biomarker, therapeutic target, or gene signature for the early diagnosis of the disease. Intellectual disability is a neurodevelopmental disorder that affects at the fetal stage. Timely diagnosis of the disease can help in preventing severe neurodevelopmental delay in the child. In the current study, meta-analysis approach was applied for the identification of the DEGs in patients of intellectual disability disorder. 6 intellectual disability datasets were retrieved from the GEO database of NCBI and were subjected to quality check, trimming, and alignment. Post-alignment, featureCounts was used to form a raw gene count file for differential analysis. The differentially expression genes were analyzed using the EdgeR statistical package of R Studio. The genes which had an FDR p-value less than 0.05 and log2foldchange greater than 0 were considered as the upregulated and significantly expressed genes. The study found MTRNR2L1, PAPSS2, L1CAM, IGLV1-47, IGLV3-19, and IGKV1-16 genes to be upregulated in the patient sample. These genes can thus play an important role in the progression of intellectual disability disorder that facilitates early diagnosis of the disease.

Alzheimer’s Disease (AD) patients suffer from circadian rhythm alterations involving sleep, thermoregulation, and movement activity disorders. The latter affects their daily patterns of physical activity (PA) and willingness to perform voluntary exercise, impeding benefit from routine PA practice. Neuropsychiatric symptoms (NPS) have been postulated to influence human physical activity engagement. However, there is no clarity on whether animal models can replicate these effects. Here, we evaluated the behavioral circadian rhythmicity of voluntary physical exercise (VPE) in a group of 14-month-old 3xTg-AD animals of both sexes at advanced stages of the disease and compared their performance according to the presence of NPS-like symptoms. Mice (n=9 females and n=7 males) were provided with an in-cage running wheel for 30 days with daily control of the diurnal and nocturnal amount of VPE performed. Using a Linear Mixed Model Analysis, we found that all animals kept similar nocturnal patterns of VPE. However, sex-dependent differences associated with previous novelty inhibition (NI) response, an NPS-like symptom frequently observed in this model, were found during diurnal periods. Thus, males with high NI showed significantly higher levels of VPE compared with high NI females. No sex differences were found in low NI animals. Our results suggest that the influence of NPS-like symptoms in VPA engagement may vary depending on the sex of 3xTg-AD mice. Further studies are needed to help elucidate molecular and genetic factors associated with these differences.

Olena G. Aliyeva, Igor F. Belenichev, Olena O. Popazova, Galina A. Zidrashko

Despite the significant advances in modern medicine, the problem of perinatal hypoxic CNS damage in children occupies one of the leading places in modern neonatology. Hypoxic damage to the fetal brain is the cause of delayed psycho-linguistic and motor development, mental insufficiency, movement disorders, cerebral palsy, disability and severe cases of neonatal mortality. Chronic prenatal hypoxia (PH) leads to biochemical and structural changes in the developing brain and, as a consequence, to the pathological development of the fetal brain, to the development of neurological deficit not only immediately after birth, but also in the late periods of postnatal ontogenesis. The protein factors identified in recent decades, which are involved in the mechanisms of urgent and long-term adaptation to hypoxia (HIF1), can serve as specific targets for pharmacological action, opening up promising opportunities for the search for new effective drugs for the treatment of hypoxic CNS lesions in children.

The aim of the research: to study the ability of a number of drugs (cerebrocurin, angiolin, glutoredoxin, thiotriazoline, L-arginine, mexidol and piracetam) to modulate the level of HIF-1α expression in the cerebral cortex of rats after chronic PH.

Materials and methods: The studies were carried out on 90 male rats of two months of age, obtained from females, in which, from the 16th day of pregnancy, chronic PH was modeled in the offspring. Newborn animals were divided into 9 groups: 1st – intact animals obtained from females with normal physiological pregnancy, which received 1 ml of physiological solution; 2nd – control animals after PH, 3-9 groups – animals after PH, which after birth were intraperitoneally injected with the drug in an effective dose (cerebrocurin – 150 μl / kg, piracetam – 500 mg / kg, angiolin 50 mg / kg, thiotriazoline – 50 mg / kg, mexidol –
100 mg / kg, L-arginine – 200 mg / kg, glutoredoxin 200 μg / kg, i. p).

Real-time reverse transcription polymer chain reaction (RT-PCR) was used to assess the state of HIF-1α expression. The results of the study were processed using the statistical package of the licensed program "STATISTICA for Windows 6.1". The significance of differences between the experimental groups was assessed using the nonparametric Mann-Whitney U-test. Differences with a significance level of more than 95% (p<0.05) were considered significant.

Results: It was found that in animals after PH, the expression level of HIF-1α mRNA is 0.331±0.0002 c.u., which is 3 times lower than in intact animals. Analysis of the results of the prolonged action of the studied preparations on the level of HIF-1α mRNA expression shows that the use of the studied preparations led to an increase in the level of HIF-1α mRNA expression, except for animals receiving L-arginine (0.37±0.001 c.u.). Cerebrocurin increased this indicator by 15.8 times (5.24±0.002 c.u.), piracetam – by 82% (0.603±0.0003 c.u.), angiolin – by 13.9 times (4,61 ± 0,004 c.u.), glutoredoxin – 8.5 times (2.80±0.002 c.u.), thiotriazoline – 6.2 times (2.06±0.001 c.u.), mexidol – 2, 3 times (0.77±0.006 c.u.). The indices of HIF-1α mRNA expression in rats after administration of cerebrocurin and angiolin are maximal and significantly exceed those of all experimental groups.

The conducted studies show that modeling of prenatal hypoxia and its pharmacological correction change the pattern of HIF-1α mRNA expression. An increase in the expression of HIF-1α mRNA directly indicates the activation of certain genes of the cellular genome associated with the action of stimulating signals on the activation of adaptive-compensatory intracellular mechanisms in cells in response to the harmful effects of PH.

Conclusions: Thus, HIF-1α is a promising target for neuroprotection after PH exposure. Cerebrocurin and angiolin can be considered as promising agents for correcting the negative consequences of chronic PH in newborns.

Epidermolysis Bullosa (EB) is a chronic disease with multiple clinical presentations depending on the subtype, characterized by skin and tissues structural fragility resulting in lesions. The low prevalence contributes to the lack of knowledge of the disease by the general population and the health sector. The disorder's heterogeneity adds challenges to describing psycho-social affectations. Therefore, our current international project searches for reference models for children and young people with EB and the elaboration of a guidebook with different life stories to learn about skills and strategies proven to help to achieve personal/professional success despite the EB condition. In the present work, a qualitative and phenomenological interview with Karen Puga, an expert adult patient with dystrophic EB from Mexico, explored several social dimensions/ages affected in EB and their impact on self-esteem. The semistructured interview depicted several life events and experiences related to her psycho-social maturation that the patient identified as the most negative or positive. The most severe obstacles were experienced during childhood in the scholar scenario. However, some of those classmates later became friendly adults, providing evidence of the temporality of some adverse life events and the relevance of maturation and resilience processes, both of herself and her counterparts. Her parents' professional profiles (nurses) and the essential role of her sister were described as foundational stones of well-being and self-esteem. Multidimensional understanding of affective relationships and sexuality and positive engagement in professional activities illustrated the development of positive dimensions of her adulthood despite the complexity of psycho-social factors in EB.

Background: Recent studies indicate that Aluminium toxicity may lead to cognitive impairment via neurodegeneration. Neurodegeneration is a common adverse effect of aging along with lifestyle and heavy metal toxicity. Literature revels that Aluminium Chloride mediated cognitive impairment is an established animal model of Alzheimer’s Disease (AD). Vitamin K2 (Menaquinones) helps to improve bone-health and prevent coronary calcification. When ingested in adequate amounts, it can decrease the oxidative stress and inflammation.

Aims and Objective: The objective of this study is to do a preliminary determination of the use of Vitamin K2 as therapeutics against Aluminium Chloride associated cognitive impairment.

Methodology: Neurodegeneration was induced in Swiss albino mice by administering Aluminium Chloride for 3 weeks. Behavioral studies including Elevated plus Maze (EPM), Passive Avoidance test, Morris water maze (MWM) and Novel object recognition (NOR) were performed to analyze the change in cognition. In the treatment group, Vitamin K2 was administered for 3 weeks in conjunction with Aluminium Chloride (3 weeks). Histopathological slides of hippocampal area were prepared for all the animal groups using H & E staining.

Results: Vitamin K2 treatment on Aluminium Chloride administered animals led to significant decrease (p<0.001) in transfer latency and increase (p<0.05) in step down latency compared to only Aluminium Chloride treated animals. Similarly time spent in the target quadrant in MWM test and preference for novel object (NOR) was significantly higher (p<0.001) for Vitamin K2 + Aluminium Chloride treated group as compared to animals in the disease control group (Aluminium Chloride treated only).

Discussion and Conclusion: Neurobehavioural and histopathological slides show that administration of Vitamin K2 may reverse the Aluminium Chloride-associated cognitive impairment in mice. This results suggest that Vitamin K2 may be protective against AD-associated neurodegeneration.

The Solitonic Windkessel model [1], which is successful for explaining the intracranial aneurysmal rupture based on the Windkessel-type hemodynamic circulation modeling, is employed for explaining intracranial aneurysmal rupture, as well as several kinds of hemorrhage. In this paper, much attention is paid to the appearance of resonance, and the hemorrhage is shown to arise from the resonance.

[1] H. Ujiie, Y. Iwata, Solitonic Windkessel model for intracranial aneurism, Brain Sciences, in press, 2022.

The resection of intracranial tumors in cerebellopontine angle area such as acoustic neuroma leads to fractures of the middle fossa and mastoid, often causing peripheral facial paralysis. The injury of Facial Nerve is the immediate cause. Studies have shown that cortical neurons repaired by peripheral nerve transfer could contribute to functional remodeling of injured nerve. Hence, nerve anastomosis is an effective method to establish nerve regeneration pathway. Current treatments include end-to-end and side-to-end hypoglossal-facial nerve anastomosis (HFA) and masseteric-facial nerve anastomosis (MFA). HFA needs to cover a relative longer distance between hypoglossal and facial nerves, complicated with either secondary dystonia or synkinetic movements that end up with a bad prognosis. Masseteric and facial nerves are located more closely with a better match in diameter, and therefore less complications in both donor and recipient sites could be expected. As reported, patients subjected to end-to-end MFA regained a normal facial function and good symmetry at about 12 months after surgery. Repetitive transcranial magnetic stimulation (rTMS) applies continuously adjustable magnetic field through repeated stimulation to achieve cumulative methods that has been successfully used in poststroke rehabilitation. However, whether rTMS can be used in promoting facial recovery from paralysis in patients after MFA remains to be explored. Here we aimed to verify the accelerated recovery from facial paralysis with a novel form of rTMS, individual-target TMS (IT-TMS), in patients after end-to-end MFA.

Mediator-specific components of functional neuronal networks underlie the study of brain functions in normal and pathological conditions. In the memory consolidation problem, cholinergic projection systems of the neocortex and hippocampus are intensively studied unlike the barely studied interneurons. We aimed to evaluate the role of both cholinergic projection neurons and interneurons of the neocortex and hippocampus at an early stage of spatial memory consolidation (2s1) in normal and chronic brain hypoperfusion conditions. Control rats and rats subjected to permanent two-vessel occlusion were trained with the Morris water maze, and the activity of membrane-bound and water-soluble choline acetyltransferase was evaluated in the sub-fractions of ‘light’ and ‘heavy’ synaptosomes of the neocortex and hippocampus, in which the presynapses of cholinergic projections and interneurons, respectively, are concentrated. Animals were ranked into quartiles according to the abilities to 2s1 performance. We found: (1) quartile-dependent cholinergic composition of 2s1 function and dynamics of cholinergic synaptic plasticity under cerebral hypoperfusion; (2) cholinergic hippocampal interneurons are necessary for successful 2s1 consolidation; (3) cholinergic neocortical interneurons and projections can be critical for 2s1 consolidation in less learning rats. We conclude that targeted modulation of cholinergic synaptic activity in the hippocampus and neocortex can be effective in reversing the cognitive disturbance of cerebral hypoperfusion. We discuss the possible ways to restore the impaired spatial memory 2s1 under cerebral hypoperfusion.

TS - related tics are largely challenging to eliminate. Heat has, in some cases, reduced compulsive symptoms in TS. However, prior reports have produced opposing results.

At 24 years of age, a man suffering with Gilles de la Tourettes Syndrome presented with the inability to carry glass bottles for fear that he might drop them due to tics.

He attempted to mitigate his tics through heat exposure, barring the knowledge or approval of his medical providers. He believed this would contribute to remission of tics by altering his dopamine production. The man entered a hot tub of 103-104 degrees F for an estimated period of 3-4 hours.

After about 2 hours, following the prolonged heat exposure, his tics subsided. He retained symptoms of extreme dehydration including cramps in extremities, pinkish urine, and general feelings of somatic weakness.

Examinations at times 1 month and 11 months following the remission demonstrated improvements of his condition when compared to data 6 months prior to heat exposure.

This remission of tics was sustained over a period of 3 years. At 27 years of age, a tetanus immunization led to an exacerbation of his compulsive symptoms. This was the worst episode he had experienced to date, which continued for two weeks. Gradually, his tics became mild again.

At 29 years of age, he used Δ⁹-tetrahydrocannabinol (THC) as a vaporized inhalant on daily basis.

The man, now 36 years of age, is doing well and continues to use vaporized THC. He is working 70 hours a week as reported during a follow-up research examination.

The man is hesitant to receive additional immunizations due to his exacerbation of tics following the tetanus immunization at 27 years of age. Therefore, he has not received a COVID-19 vaccination, but was not severely affected upon contraction of the virus.