Neurology and Neurobiology

Journal Information
ISSN / EISSN : 2613-7828 / 2613-7828
Published by: Science Repository OU (10.31487)
Total articles ≅ 58
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Latest articles in this journal

Melissa Johnson, Mohammed Teleb
Published: 24 August 2022
Neurology and Neurobiology, Volume 2022, pp 1-4; https://doi.org/10.31487/j.nnb.2022.03.01

Abstract:
Introduction: This review article outlines the clinical symptoms associated with isolated occlusions in the major branches of the anterior, middle, and posterior cerebral arteries. Methods: Review article Conclusion: A comprehensive understanding of isolated branch infarcts will deepen clinical acumen, aid in precise infarct localization, and optimize diagnostic management.
Andrew Larner
Published: 19 August 2022
Neurology and Neurobiology, Volume 2022, pp 1-4; https://doi.org/10.31487/j.nnb.2022.03.02

Abstract:
Functional amnesia, also known as dissociative amnesia, psychogenic amnesia, or mnestic block syndrome, is a rare disorder which, although clinically heterogeneous, is most often characterised by dense retrograde amnesia mainly affecting the episodic-autobiographical domain but with relative preservation of anterograde memory function, a pattern dissimilar to that seen in other amnesic disorders. The pathogenesis of functional amnesia remains unknown. Here, appeal is made to the study of artificial neural networks in the hope that, as in other mnestic disorders, this might give insight into the mechanisms underpinning functional amnesia. Specifically, the observation of catastrophic forgetting or catastrophic interference occurring in artificial neural networks, that is the abrupt and complete loss of previously learned information when learning new information, is extended to the human nervous system to develop a novel hypothesis: the Catastrophic Forgetting Hypothesis of functional amnesia.
Dong Y Han, Michael W. Williams, Justin E. Karr, Alyssa M. Day, Amanda C. Glueck, Siddharth Kapoor
Published: 8 August 2022
Neurology and Neurobiology, Volume 2022, pp 1-7; https://doi.org/10.31487/j.nnb.2022.02.04

Abstract:
This study examined the relationships between post-traumatic headache (PTH) and mental health symptoms after concussions to inform adolescent concussion management. Headache is the most common complaint following adolescent concussion. In this sample of 123 adolescents with concussion, there was a 5-fold increase in odds of clinically elevated anxiety, as well as increased mental health symptoms (anxiety, depression, anger, and disruptive behaviours), among adolescents with PTH relative to those without PTH. Adolescents with headache following concussions are vulnerable to worse mental health outcomes, particularly anxiety, and may benefit from routine monitoring of mental health symptoms for early detection and intervention.
Dong Y Han, Madeline Aulisio, Sandro Pasagic, Amanda C. Glueck, Timothy J. Ainger
Published: 5 August 2022
Neurology and Neurobiology, Volume 2022, pp 1-3; https://doi.org/10.31487/j.nnb.2022.02.03

Abstract:
A 53-year-old male with history of traumatic brain injury (TBI) presented with localized dissociative amnesia following a second head injury. While memory loss due to TBI is present in the literature, presentations of this type are very rare. Although fully independent in activities of daily living, this patient demonstrated severe deficits in visual memory and processing speed upon neurocognitive evaluation. Effort testing was unremarkable. Increased awareness and study of memory loss following TBI can contribute to enhanced understanding and improved care for patients experiencing these deficits. The authors present this unique case’s profile, clinical history, and discuss their findings.
Rossi Evelyn Barrientos Castillo, Manuel Encarnacion Ramirez, Gerald Musa, Renat Nurmukhametov, Boris O. Igorevich
Published: 11 July 2022
Neurology and Neurobiology, Volume 2022, pp 1-3; https://doi.org/10.31487/j.nnb.2022.02.02

Abstract:
Background: ‘Brain tissue out’ (BTO) is used here to describe traumatic acute extracranial cerebral herniation, an extreme manifestation of severe TBIs. Case Description: We report a case of a 15-year-old victim of a severe head injury who was brought with acute extracranial cerebral herniation ‘brain tissue out’. We review the current literature and evidence of this exceedingly rare presentation. Conclusion: 'Brain tissue out' is a rare form of severe head injury with a very poor prognosis. The possible catastrophic short long-term effects of this injury warrant further attention to clarify the underlying mechanisms and to identify its management guidelines.
Thomas G. Bowman, Monica R. Lininger, Amanda O. Esquivel, Katherine M. Breedlove
Published: 2 May 2022
Neurology and Neurobiology, Volume 2022, pp 1-7; https://doi.org/10.31487/j.nnb.2022.02.01

Abstract:
Neurocognitive changes have been found in participants of contact sports without documented concussions, raising concerns regarding the long-term consequences of subconcussive head impacts in sport. However, sex comparisons of neurocognitive change without reported concussions have not been completed for soccer or lacrosse athletes. Our purpose was to determine changes in clinical measures of cognitive function in uninjured collegiate lacrosse and soccer players. Men’s soccer (N=23), women’s soccer (N=36), men’s lacrosse (N=28) and women’s lacrosse (N=31) players wore xPatch head impact monitoring sensors for all practices and games. Sensors measured peak linear accelerations and peak rotational accelerations, allowing for daily density calculations. Participants completed the Sport Concussion Assessment Tool 3 and Immediate Post-Concussion and Cognitive Testing at the beginning and end of the season. For women, multiple statistically significant relationships were identified [decreased reaction time with increased cumulative peak linear acceleration (rs=-0.30, P=0.03), peak linear acceleration daily density (rs=-0.31, P=0.04), and peak rotational acceleration daily density (rs=-0.31, P=0.03) and also Immediate Post-Concussion and Cognitive Testing symptom change increased with increased cumulative peak linear acceleration (rs=-0.38, P=0.008) and cumulative peak rotational acceleration (rs=-0.37, P=0.009)]. For men, cognitive change scores, specifically concentration, had the only statistically significant relationship with cumulative peak rotational acceleration (rs=0.32, P=0.02). Men had a greater number of changes over the course of the season compared to women; however, the changes did not appear related to head impact biomechanics. Women had many statistically significant correlations between head impacts and deterioration in some constructs, especially symptoms.
Zhidan Liu, Xiaoyan Li, Ying Zhao, Chuang Zhao, Chunlan Chen, Zunyuan Li, Wenge Huo
Published: 11 February 2022
Neurology and Neurobiology, Volume 2022, pp 1-9; https://doi.org/10.31487/j.nnb.2022.01.01

Abstract:
Background: Bell’s palsy is a widespread disease of the peripheral nervous system which causes not only physical disorders but also mental suffering as well. However, the etiological factor of Bell’s palsy is still unclear. The present study aimed to search for potential influencing factors by identifying the key genes and long non-coding RNAs (lncRNAs) involved in patients with Bell’s palsy using RNA-Seq data based on bioinformatics tools. Methods: Differentially expressed genes (DEGs) and differentially expressed lncRNAs (DELs) in patients before and after therapy, and that in normal control group were identified. The competing endogenous RNAs (ceRNAs) regulatory network was constructed by integrating lncRNA-mRNA pairs, miRNA-mRNA regulatory pairs, and miRNA-lncRNA pairs using Cytoscape. The Gene Ontology (GO) functions and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways analyses of DEGs and DELs were evaluated to explore their functions. The targeted corresponding genes and pathogens were verified by ELISA and q-PCR. Results: In the present study, hub proteins such as CXCR2 and IL1R1 in PPI network and 1039 lncRNA-mRNA co-expression pairs (eg., CYYR1-AS1-MDM2) were identified. 739 miRNA-mRNA pairs (eg., hsa-miR-147a-IL1R1), 255 miRNA-lncRNA pairs, and 363 mRNA-lncRNA co-expression pairs were included in ceRNA regulatory network. Meanwhile, CYYR1-AS1 was enriched into most pathways, including Epstein-Barr virus (EBV) infection. Subsequently, validation of neuroinflammation relevant IL1R1 and EBV showed that IL1R1 was upregulated in the serum of patients with Bell’s palsy before therapy, while EBV was not found among them. Conclusion: We hypothesized that etiological factor of Bell's palsy correlate to complex miRNA-lncRNA-mRNA interacting networks and IL1 might be involved in inflammation and immune regulation in the onset of Bell's palsy.
Dianne E. Godar
Published: 31 December 2021
Neurology and Neurobiology, Volume 2021, pp 1-7; https://doi.org/10.31487/j.nnb.2021.04.02

Abstract:
Because the concordance rate between identical twins is only 88%, an environmental factor must cause autism spectrum disorder (ASD). Furthermore, when identical twins share ASD, it is to varying degrees suggesting different prenatal environments exist, which occurs when identical twins have separate placentas (~30% of the time). Placental inclusions are predictive of ASD along with excessive increases in extra-axial cerebral spinal fluid (CSF) detected by MRI in the brains of 6- and 12-month-old infants later diagnosed at 2 years with ASD. The human papillomavirus (HPV) can infect the trophoblast cells of placentas and transmit to the fetus where it infects the epithelial cells of the choroid plexus, a centrally located lining inside the brain responsible for producing CSF via the SLC4A10 gene product. HPV causes epigenetic changes, deletions, and duplications of genes, and besides its characteristic methylation patterns, the SLC4A10 gene was found to be increased in children with ASD. Moreover, male placentas implant close to the cervix (low-lying) three times more often than female placentas paralleling the ASD ratio of ~3:1 (boys to girls). Finally, the Australian HPV vaccination programme that began in 2007 might explain why the 0-4 yr. ASD incidence did not increase from 2010 to 2015.
Reham M. Abdel-Kader, Engy A Fadel
Published: 2 December 2021
Neurology and Neurobiology, Volume 2021, pp 1-10; https://doi.org/10.31487/j.nnb.2021.04.01

Abstract:
Background: Mitochondrial biogenesis has been recently implicated to play an important role in Alzheimer’s disease (AD). Recently it has been reported that brains of AD patients show reduced expression in major genes and proteins such as PGC-1α involved in mitochondrial biogenesis. This led to the idea that enhancing mitochondrial biogenesis in AD, might represent a plausible strategy for AD treatment. Pyrroloquinoline quinone (PQQ) has been recently implicated in enhancing cognitive functions during aging; however, its effect on mitochondrial biogenesis in neuroinflammatory AD mouse model was not previously examined. Objective: The aim of this project was to test the cognitive enhancement effect of PQQ in a neuroinflammatory mouse model mimicking AD, and whether PQQ is able to activate mitochondrial biogenesis in brains of our AD mouse model. Methods: Neuroinflammatory AD mouse model was developed by Lipopolysaccharide (250 g kg-1 body weight, i.p) injection for 7 days, followed by daily PQQ treatment (10 mg kg-1 body weight) on days 4-7. Cognitive functions were assessed using Y-Maze, Water-Maze and object recognition tests. Neurodegeneration was evaluated using H&E. Finally, mitochondrial proteins were measured using immunohistochemistry. Results: PQQ treatment improved spatial recognition and working memory. PQQ treated mice brains showed decreased levels of neurodegeneration. Moreover, their brains showed greater amounts of both PGC-1α and the mitochondrial-membrane-bound protein cytochrome-c, indicating enhancement of mitochondrial biogenesis. Conclusion: This study demonstrates the ability of PQQ to improve memory in neuroinflammatory AD model via enhancing mitochondrial biogenesis, which may represent an alternative mechanistic approach for treating AD.
Jason C. O’Connor, Grace A. Porter
Published: 25 September 2021
Neurology and Neurobiology, Volume 2021, pp 1-10; https://doi.org/10.31487/j.nnb.2021.03.03

Abstract:
Chronic stress is a well-known risk factor in major depressive disorder and disrupts the kynurenine and serotonin pathways of tryptophan metabolism. Here, we characterize the temporal central and peripheral changes in tryptophan metabolism and concomitant depressive-like behavioural phenotype induced during the progression of chronic unpredictable stress (CUS). Mice were exposed to 0, 10, 20, or 30 days of CUS followed by a panel of behavioural assays to determine depressive-like phenotypes. Immediately after behavioural testing, plasma and brain tissue were collected for metabolic analysis. While anhedonia-like and anxiety-like behaviours were unaffected by stress, nesting behaviour and cognitive deficits became apparent in response to CUS exposure. While CUS caused a transient reduction in circulating quinolinic acid, no other tryptophan metabolites significantly changed in response to CUS. In the brain, tryptophan, kynurenine, picolinic acid, and 5-hydroxyindoleacetic acid concentrations were significantly elevated in CUS-exposed mice compared with non-stress control animals, while kynurenic acid, xanthurenic acid, and serotonin decreased in CUS-exposed mice. Metabolic turnover of serotonin to the major metabolite 5-hydroxyindoleacetic acid was markedly increased in response to CUS. These results suggest that CUS impairs hippocampal-dependent working memory and enhances nascent nesting behaviour in C57BL/6J male mice, and these behaviours are associated with increased brain kynurenine pathway metabolism leading to accumulation of picolinic acid and a significant reduction in serotonin levels.
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