NeuroSci, Volume 3, Issue 1 (March 2022) – 11 articles

Reactive oxygen species (ROS) have emerged as regulators of key processes supporting neuronal growth, function, and plasticity across lifespan. At normal physiological levels, ROS perform important roles as secondary messengers in diverse molecular processes such as regulating neuronal differentiation, polarization, synapse maturation, and neurotransmission. In contrast, high levels of ROS are toxic and can ultimately lead to cell death. Excitable cells, such as neurons, often require high levels of metabolic activity to perform their functions. As a consequence, these cells are more likely to produce high levels of ROS, potentially enhancing their susceptibility to oxidative damage. In addition, because neurons are generally post-mitotic, they may be subject to accumulating oxidative damage. Thus, maintaining tight control over ROS concentration in the nervous system is essential for proper neuronal development and function. We are developing a more complete understanding of the cellular and molecular mechanisms for control of ROS in these processes. This review focuses on ROS regulation of the developmental and functional properties of neurons, highlighting recent in vivo studies. We also discuss the current evidence linking oxidative damage to pathological conditions associated with neurodevelopmental and neurodegenerative disorders. Full article

The impact of Moyamoya Disease (MMD) on cognition inadult Caucasian patients has not yet been thoroughly investigated. The current study is the first to present detailed neuropsychological data on a series of Greek patients with MMD. A group of eight patients was assessed with an extensive neuropsychological battery, including measures of episodic memory, working memory, executive functions, language, and social cognition. The results indicated that MMD may be characterized by a trichotomous neurocognitive profile, characterized by prominent impairment in working memory, executive functions, and social cognition. Overall, we stress the need for a thorough cognitive evaluation of MMD patients and further highlight the potential importance of social cognition in this particular disease. Possible associations between the three impaired cognitive domains in our group are also discussed. Full article

Background: Schizophrenia is a heterogeneous neuropsychiatric disorder, categorized by positive, negative, and cognitive symptoms. In trying to improve the diagnosis and treatment of schizophrenia, researchers have turned to “dual hit” models of schizophrenia that are able to reproduce all symptoms of the disorder. The main objective of this protocol is to present a transparent process on how we plan to review the existing international literature on the effectiveness of “dual hit” models used to induce schizophrenia on rodents. Methods: Literature search strategies will be developed using medical search headings (MeSH). The MEDLINE (PubMed), EMBASE, and Google Scholar databases will be used to search for electronically published studies. We will search for studies involving inducing schizophrenic symptoms using “dual hit” rodent models (post-weaning social isolation and NMDA receptor antagonist). Studies will be screened by titles, abstracts, keywords, and synonyms followed by identifying the full-text articles. All studies that will pass quality assessment will be included. Data will be extracted by two authors independently and in duplicate from each eligible study to ensure that there is consistency between reviews. If the design and comparator are sufficiently homogenous for all studies, a meta-analysis will be conducted using a random-effect model. Discussion: The results of this review will contribute to the development of new “dual hit” models that will be able to characterize schizophrenia symptoms better. It will also shed light to researchers on new developments that need to be made in improving animal models of schizophrenia. Full article

Advances in our understanding of the genetics of mental disorders (MD) have contributed to a better understanding of their pathophysiology. Nonetheless, several questions and doubts remain. Recent research has focused on the role of the environment in developing mental disorders, and the advent of neuroscientific methodologies has opened up new avenues of inquiry. However, the mechanism by which childhood stress affects neurodevelopment via mechanisms, such as gene-environment interactions and epigenetic regulation leading to diseases in adulthood, is unclear. This paper aims to review the evidence on the role of early life stress and parental psychopathology in the pathophysiology and clinical expression of MD. Methodology: The study will conduct a comprehensive systematic review using medical search terms (MeSH). Electronic searches for published studies will be performed using the MEDLINE (PubMed), EMBASE, Scopus, PsychINFO, Web of Science, and Google Scholar databases. We will look for research on the neuroplasticity effects of early life stress on development and review articles that evaluate cognitive functions and the development of psychopathology and MD. Before identifying full-text articles, several studies will be filtered based on titles, abstracts, keywords, and synonyms. Publications to be included in the review will be assessed for quality and consistency before inclusion. Data will be extracted independently and duplicated by two authors from each eligible study to ensure consistency between reviews. All databases will be searched from inception until July 2021 and will be limited to human studies. The search will be limited only to publication in the English language and any publication that can be converted to English. Discussion and Conclusions: The findings of this review will meticulously articulate the effects of childhood adversity, such as ELS and parental psychopathology on cognitive development and neuroplasticity. Full article

An animal neural system ranges from a cluster of a few neurons to a brain of billions. At the lower range, it is possible to test each neuron for its role across a set of environmental conditions. However, the higher range requires another approach. One method is to disentangle the organization of the neuronal network. In the case of the entorhinal cortex in a rodent, a set of neuronal cells involved in spatial location activate in a regular grid-like arrangement. Therefore, it is of interest to develop methods to find these kinds of patterns in a neural network. For this study, a square grid arrangement of neurons is quantified by network metrics and then applied for identification of square grid structure in areas of the fruit fly brain. The results show several regions with contiguous clusters of square grid arrangements in the neural network, supportive of specialization in the information processing of the system. Full article

Post-traumatic Stress Disorder is a chronic condition that occurs following a traumatic experience. Information processing models of PTSD focus on integrating situationally triggered sensory-emotional memories with consciously accessible autobiographical memories. Review of the nature of implicit memory supports the view that sensory-emotional memories are implicit in nature. Dissociation was also found to be associated with the development and severity of PTSD, as well as deficits in autobiographical memory. Moreover, disorganized attachment (DA) was associated with greater degrees of dissociation and PTSD, and like the defining neural activation in PTSD, was found to be associated with basal ganglia activity. In addition, subcortical neuroception of safety promotes a neurophysiological substrate supportive of social engagement and inhibition of fear-based responses. Furthermore, activation of representations of co-created imagined scenes of safety and secure attachment are associated with increases in this neurophysiological substrate. Repeated priming of secure attachment imagery was associated with modification of internal working models of DA along with reductions in dissociation and recovery from complex PTSD. In conclusion, it is posited that adequate recovery from extensive trauma experiences requires more than conscious elaboration of traumatic autobiographical memories and that the application of implicit nonconscious memory modification strategies will facilitate more optimal recovery. Full article

Purpose: The main purpose of this retrospective study was to identify auditory dysfunctions related to traumatic brain injury (TBI) in individuals evaluated in an Audiology clinic. Method: Peripheral and central auditory evaluations were performed from March 2014 to June 2018 in 26 patients (14 males) with TBI. The age of the participants ranged from 9 to 59 years old (34.24 ± 15.21). Six participants had blast-related TBI and 20 had blunt force TBI. Sixteen experienced a single TBI event whereas ten experienced several. Correlation analyses were performed to verify the relationship, if any, between the number of auditory tests failed and the number, type, and severity of TBIs. Result: All participants failed at least one auditory test. Nearly 60% had abnormal results on degraded speech tests (compressed and echoed, filtered or in background noise) and 25% had a high frequency hearing loss. There was no statistically significant correlation between the number of auditory tests failed and the number, type, and severity of TBIs. Conclusion: Results indicated negative and heterogenous effects of TBI on peripheral and central auditory function and highlighted the need for a more extensive auditory assessment in individuals with TBI. Full article

Transmembrane 29 (Tmem29) gene with unknown function is a gene located on the X chromosome of the mouse genome. The gene showed differential expression in the Vannucci neonatal hypoxic-ischemic mouse brain model. We found the gene expresses with different molecular forms, including a group of long non-coding RNA forming a family of transcripts. It was predominantly expressed in the testes, brain, and kidney of mouse. In vitro identification and functional characterization were carried out in Neuro2a cells. Using fluorescence microscopy, Tmem29 protein was found to be constitutively expressed in mouse cell lines of different origins. Oxygen glucose deprivation (OGD) induced apoptotic cell death in Neuro2a cells and was confirmed by activations of caspase 3. Tmem29 protein was found to be associated with cell death especially at the time points of caspase 3 activations. A similar response was obtained in glucose deprivation (GD) cultures suggesting Tmem29 response to a common mechanism induced by OGD and GD. Downregulation of Tmem29 was induced by OGD and GD, further validating its response to hypoxia-ischemia (HI) insults. Our findings contributed to further understanding of molecular events after hypoxic-ischemic insults and opens new avenues for developing protective and therapeutic strategies for hypoxic-ischemic encephalopathy or even pathological programmed cell death. Full article

(1) Background: As a natural carbohydrate, sialic acid (SA) is helpful for brain development, cognitive ability, and the nervous system, but there are few reports about the effect of SA on Alzheimer’s disease (AD). (2) Method: The present study evaluated the effect of SA on cognitive ability, neuronal activity, Aβ formation, and tau hyperphosphorylation in a double transgenic AD (2×Tg-AD) mice model. The 2×Tg-AD mice were randomly divided into four groups: the AD control group, 17 mg/kg SA-treated AD group, 84 mg/kg SA-treated AD group, and 420 mg/kg SA-treated AD group. Mice from all four groups were fed to 7 months of age for the behavioral test and to 9 months of age for the pathological factors investigation. (3) Results: In the Morris water maze, the escape latency significantly decreased on the fifth day in the SA-treated groups. The number of rearing and crossing times in the open field test also increased significantly, compared with the control group. SA treatment significantly reduced amyloid β-peptide (Aβ) and nerve fibers and increased the number of Nissl bodies in the brain of AD mice. (4) Conclusions: SA reduced the neuron damage by reducing Aβ and inhibited tau protein hyperphosphorylation, which improved the cognitive ability and mobility of AD mice. Full article

The blood-spinal cord barrier (BSCB) has been long thought of as a functional equivalent to the blood-brain barrier (BBB), restricting blood flow into the spinal cord. The spinal cord is supported by various disc tissues that provide agility and has different local immune responses compared to the brain. Though physiologically, structural components of the BSCB and BBB share many similarities, the clinical landscape significantly differs. Thus, it is crucial to understand the composition of BSCB and also to establish the cause–effect relationship with aberrations and spinal cord dysfunctions. Here, we provide a descriptive analysis of the anatomy, current techniques to assess the impairment of BSCB, associated risk factors and impact of spinal disorders such as spinal cord injury (SCI), amyotrophic lateral sclerosis (ALS), peripheral nerve injury (PNI), ischemia reperfusion injury (IRI), degenerative cervical myelopathy (DCM), multiple sclerosis (MS), spinal cavernous malformations (SCM) and cancer on BSCB dysfunction. Along with diagnostic and mechanistic analyses, we also provide an up-to-date account of available therapeutic options for BSCB repair. We emphasize the need to address BSCB as an individual entity and direct future research towards it. Full article