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Biomedicines
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Brain Injury and Neurodegeneration: Molecular, Functional, and Translational Approach 2.0
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Brain Injury and Neurodegeneration: Molecular, Functional, and Translational Approach 2.0

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 42164

Special Issue Editors

Dr. Kumar Vaibhav

E-Mail Website
Guest Editor
Department of Neurosurgery, Augusta University, Augusta, GA 30912, USA
Interests: traumatic brain injury; stroke; hemorrhages; Alzheimer’s disease; Parkinson’s disease; neuroinflammation; macrophages; neutrophils; t-cells; metabolism; cannabinoids; cannabinoid receptors; ischemic conditioning; edema; apoptosis; scavenging receptors; innate immune cells; innate lymphoid cells; cycloxygenase; mitochondria; RBCs; miRNA
Special Issues, Collections and Topics in MDPI journals
Dr. Pankaj Ahluwalia

E-Mail Website
Guest Editor
Department of Pathology, Medical College of Georgia, Augusta University, Augusta, GA 30912, USA
Interests: pathology; COVID-19, neutrophils; lymphoid cells; genome sequencing; nucleic acid; testing; cancer
Special Issues, Collections and Topics in MDPI journals
Dr. Pankaj Gaur

E-Mail Website
Guest Editor
Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC 20007, USA
Interests: brain functions; traumatic brain injury; stroke; hemorrhages; alzheimer’s disease; Parkinson’s disease; Neuroinflammation
Special Issues, Collections and Topics in MDPI journals
Dr. Meenakshi Ahluwalia

E-Mail Website
Guest Editor
Department of Pathology, Augusta University, Augusta, GA 30912, USA
Interests: pathology; traumatic brain injury; macrophages; t-cells; cannabinoids; oxidative stress; pesticides; genetic alterations; genome sequencing; nucleic acid; imaging
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

With the advance of neuroscience research, we have come across different kinds of brain pathologies such as traumatic brain injury (TBI), hypoxic/hypobaric insults, hemorrhages, stroke, and neurological disorders such as Parkinson’s and Alzheimer’s diseases. Any insult to brain (mild or acute) is multifactorial and initiates a cascade of inflammation, necrotic, and apoptotic pathways. It has long been known that insult or injury to brain may lead to neurological disorders such as Alzheimer’s and Parkinson’s disease as time elapses, and genetic or environmental factors play important roles in the progression of disease. A large body of evidence has shown that oxidative stress, mitochondrial dysfunctions, protein aggregation and phosphorylation, excessive iron accumulation in the brain, and neuro-inflammation play a pivotal role in neurodegeneration and brain injuries. The absence of a specific cure to limit injury progression after insult has spurred the scientific community to study the mechanism behind the degenerative cascade and to explore different therapeutic strategies.

 This Special Issue will provide a multidisciplinary platform for discussing the pathology and intervention of brain disorders. This issue will emphasize the psychological, behavioral, inflammatory, and molecular mechanisms in the development of new preventive and therapeutic strategies to limit brain injury and neurodegenerative disorders. This issue accepts original high-quality research articles that are not yet published or sought for publication. Please feel free to discuss with the editor.

Potential topics include but are not limited to the following:

  • Molecular and histological alterations in an injured brain;
  • Behavioral changes in an injured brain;
  • Hypoxic brain injury and the role of vasculature;
  • Traumatic brain injury: mechanism and prevention;
  • Brain injury: emotional and psychological stress;
  • Parkinson’s and Alzheimer’s disease;
  • Neurodegeneration: does it link to previous brain injury?
  • COVID-19: Are brain pathologies involved?
  • Brain insult and cognitive impairment;
  • Intracerebral hemorrhages and hypoxia;
  • Stroke-induced molecular and functional alterations;
  • Prevention of brain insult by natural molecules and pharmaceuticals;
  • Bioanalytical studies and receptor mediated mechanism of natural compounds for the prevention of different kind of brain injuries;
  • Mechanisms of action of pharmaceuticals and natural products targeting oxidative stress and neuroinflammation in injured brain;
  • Computational and genetic studies of brain injuries;
  • Brain injury: protein misfolding and mitochondrial dysfunction.

Dr. Kumar Vaibhav
Dr. Pankaj Ahluwalia
Dr. Pankaj Gaur
Dr. Meenakshi Ahluwalia
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • brain injury
  • psychological stress
  • Parkinson’s disease
  • Alzheimer’s disease
  • stroke
  • neurodegeneration
  • hemorrhages
  • hypoxia
  • neuroinflammation
  • translational approaches
  • oxidative stress
  • COVID-19
  • gut–brain axis

Related Special Issue

Published Papers (15 papers)

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Research

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14 pages, 1739 KiB  
Article
Cognitive and Cellular Effects of Combined Organophosphate Toxicity and Mild Traumatic Brain Injury
by Dor Freidin, Meirav Har-Even, Vardit Rubovitch, Kathleen E. Murray, Nicola Maggio, Efrat Shavit-Stein, Lee Keidan, Bruce A. Citron and Chaim G. Pick
Biomedicines 2023, 11(5), 1481; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines11051481 - 19 May 2023
Viewed by 1346
Abstract
Traumatic brain injury (TBI) is considered the most common neurological disorder among people under the age of 50. In modern combat zones, a combination of TBI and organophosphates (OP) can cause both fatal and long-term effects on the brain. We utilized a mouse [...] Read more.
Traumatic brain injury (TBI) is considered the most common neurological disorder among people under the age of 50. In modern combat zones, a combination of TBI and organophosphates (OP) can cause both fatal and long-term effects on the brain. We utilized a mouse closed-head TBI model induced by a weight drop device, along with OP exposure to paraoxon. Spatial and visual memory as well as neuron loss and reactive astrocytosis were measured 30 days after exposure to mild TBI (mTBI) and/or paraoxon. Molecular and cellular changes were assessed in the temporal cortex and hippocampus. Cognitive and behavioral deficits were most pronounced in animals that received a combination of paraoxon exposure and mTBI, suggesting an additive effect of the insults. Neuron survival was reduced in proximity to the injury site after exposure to paraoxon with or without mTBI, whereas in the dentate gyrus hilus, cell survival was only reduced in mice exposed to paraoxon prior to sustaining a mTBI. Neuroinflammation was increased in the dentate gyrus in all groups exposed to mTBI and/or to paraoxon. Astrocyte morphology was significantly changed in mice exposed to paraoxon prior to sustaining an mTBI. These results provide further support for assumptions concerning the effects of OP exposure following the Gulf War. This study reveals additional insights into the potentially additive effects of OP exposure and mTBI, which may result in more severe brain damage on the modern battlefield. Full article
(This article belongs to the Special Issue Brain Injury and Neurodegeneration: Molecular, Functional, and Translational Approach 2.0)
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16 pages, 1976 KiB  
Article
Temporary Occlusion of Common Carotid Arteries Does Not Evoke Total Inhibition in the Activity of Corticospinal Tract Neurons in Experimental Conditions
by Agnieszka Szymankiewicz-Szukała, Juliusz Huber, Piotr Czarnecki, Agnieszka Wiertel-Krawczuk and Mikołaj Dąbrowski
Biomedicines 2023, 11(5), 1287; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines11051287 - 27 Apr 2023
Cited by 1 | Viewed by 1264
Abstract
Temporary occlusion of the common cervical artery is the reason for ischemic stroke in 25% of patients. Little data is provided on its effects, especially regarding neurophysiological studies verifying the neural efferent transmission within fibers of the corticospinal tract in experimental conditions. Studies [...] Read more.
Temporary occlusion of the common cervical artery is the reason for ischemic stroke in 25% of patients. Little data is provided on its effects, especially regarding neurophysiological studies verifying the neural efferent transmission within fibers of the corticospinal tract in experimental conditions. Studies were performed on 42 male Wistar rats. In 10 rats, ischemic stroke was evoked by permanent occlusion of the right carotid artery (group A); in 11 rats, by its permanent bilateral occlusion (B); in 10 rats, by unilateral occlusion and releasing after 5 min (C); and in 11 rats, by bilateral occlusion and releasing after 5 min (D). Efferent transmission of the corticospinal tract was verified by motor evoked potential (MEP) recordings from the sciatic nerve after transcranial magnetic stimulation. MEPs amplitude and latency parameters, oral measurements of temperature, and verification of ischemic effects in brain slides stained with hematoxylin and eosin staining (H + E) were analyzed. In all groups of animals, the results showed that five minutes of uni- or bilateral occlusion of the common carotid artery led to alterations in brain blood circulation and evoked changes in MEP amplitude (by 23.2% on average) and latency parameters (by 0.7 ms on average), reflecting the partial inability of tract fibers to transmit neural impulses. These abnormalities were associated with a significant drop in the body temperature by 1.5 °C on average. Ten minutes occlusion in animals from groups A and B resulted in an MEP amplitude decrease by 41.6%, latency increase by 0.9 ms, and temperature decrease by 2.9 °C of the initial value. In animals from groups C and D, five minutes of recovery of arterial blood flow evoked stabilization of the MEP amplitude by 23.4%, latency by 0.5 ms, and temperature by 0.8 °C of the initial value. In histological studies, the results showed that ischemia was most prominent bilaterally in sensory and motor areas, mainly for the forelimb, rather than the hindlimb, innervation of the cortex, putamen and caudate nuclei, globulus pallidus, and areas adjacent to the fornix of the third ventricle. We found that the MEP amplitude parameter is more sensitive than the latency and temperature variability in monitoring the ischemia effects course following common carotid artery infarction, although all parameters are correlated with each other. Temporary five-minute lasting occlusion of common carotid arteries does not evoke total and permanent inhibition in the activity of corticospinal tract neurons in experimental conditions. The symptoms of rat brain infarction are much more optimistic than those described in patients after stroke, and require further comparison with the clinical observations. Full article
(This article belongs to the Special Issue Brain Injury and Neurodegeneration: Molecular, Functional, and Translational Approach 2.0)
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18 pages, 14577 KiB  
Article
Neuroinflammation, Oxidative Stress, Apoptosis, Microgliosis and Astrogliosis in the Cerebellum of Mice Chronically Exposed to Waterpipe Smoke
by Naserddine Hamadi, Sumaya Beegam, Nur Elena Zaaba, Ozaz Elzaki, Mariam Abdulla Altamimi and Abderrahim Nemmar
Biomedicines 2023, 11(4), 1104; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines11041104 - 06 Apr 2023
Viewed by 1528
Abstract
Waterpipe smoking (WPS) is prevalent in Asian and Middle Eastern countries and has recently gained worldwide popularity, especially among youth. WPS has potentially harmful chemicals and is associated with a wide range of adverse effects on different organs. However, little is known regarding [...] Read more.
Waterpipe smoking (WPS) is prevalent in Asian and Middle Eastern countries and has recently gained worldwide popularity, especially among youth. WPS has potentially harmful chemicals and is associated with a wide range of adverse effects on different organs. However, little is known regarding the impact of WPS inhalation on the brain and especially on the cerebellum. Presently, we aimed at investigating inflammation, oxidative stress and apoptosis as well as microgliosis and astrogliosis in the cerebellum of BALB/C mice chronically (6 months) exposed to WPS compared with air-exposed mice (control). WPS inhalation augmented the concentrations of proinflammatory cytokines tumor necrosis factor, interleukin (IL)-6 and IL-1β in cerebellar homogenates. Likewise, WPS increased oxidative stress markers including 8-isoprostane, thiobarbituric acid reactive substances and superoxide dismutase. In addition, compared with the air-exposed group, WPS caused an increase in the oxidative DNA damage marker, 8-hydroxy-2′-deoxyguanosine, in cerebellar homogenates. Similarly, in comparison with the air group, WPS inhalation elevated the cerebellar homogenate levels of cytochrome C, cleaved caspase-3 and nuclear factor-κB (NF-κB). Immunofluorescence analysis of the cerebellum showed that WPS exposure significantly augmented the number of ionized calcium-binding adaptor molecule 1 and glial fibrillary acidic protein-positive microglia and astroglia, respectively. Taken together, our data show that chronic exposure to WPS is associated with cerebellar inflammation, oxidative stress, apoptosis, microgliosis and astrogliosis. These actions were associated with a mechanism involving NF-κB activation. Full article
(This article belongs to the Special Issue Brain Injury and Neurodegeneration: Molecular, Functional, and Translational Approach 2.0)
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12 pages, 1300 KiB  
Article
Hypoxia Depresses Synaptic Transmission in the Primary Motor Cortex of the Infant Rat—Role of Adenosine A1 Receptors and Nitric Oxide
by Isabella Zironi and Giorgio Aicardi
Biomedicines 2022, 10(11), 2875; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10112875 - 10 Nov 2022
Viewed by 1222
Abstract
The acute and long-term consequences of perinatal asphyxia have been extensively investigated, but only a few studies have focused on postnatal asphyxia. In particular, electrophysiological changes induced in the motor cortex by postnatal asphyxia have not been examined so far, despite the critical [...] Read more.
The acute and long-term consequences of perinatal asphyxia have been extensively investigated, but only a few studies have focused on postnatal asphyxia. In particular, electrophysiological changes induced in the motor cortex by postnatal asphyxia have not been examined so far, despite the critical involvement of this cortical area in epilepsy. In this study, we exposed primary motor cortex slices obtained from infant rats in an age window (16–18 day-old) characterized by high incidence of hypoxia-induced seizures associated with epileptiform motor behavior to 10 min of hypoxia. Extracellular field potentials evoked by horizontal pathway stimulation were recorded in layers II/III of the primary motor cortex before, during, and after the hypoxic event. The results show that hypoxia reversibly depressed glutamatergic synaptic transmission and neuronal excitability. Data obtained in the presence of specific blockers suggest that synaptic depression was mediated by adenosine acting on pre-synaptic A1 receptors to decrease glutamate release, and by a nitric oxide (NO)/cGMP postsynaptic pathway. These effects are neuroprotective because they limit energy failure. The present findings may be helpful in the preclinical search for therapeutic strategies aimed at preventing acute and long-term neurological consequences of postnatal asphyxia. Full article
(This article belongs to the Special Issue Brain Injury and Neurodegeneration: Molecular, Functional, and Translational Approach 2.0)
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31 pages, 10384 KiB  
Article
Expression of Amyloid Precursor Protein, Caveolin-1, Alpha-, Beta-, and Gamma-Secretases in Penumbra Cells after Photothrombotic Stroke and Evaluation of Neuroprotective Effect of Secretase and Caveolin-1 Inhibitors
by Svetlana Sharifulina, Andrey Khaitin, Valeria Guzenko, Yuliya Kalyuzhnaya, Valentina Dzreyan, Alexandr Logvinov, Natalia Dobaeva, Yan Li, Lei Chen, Bin He and Svetlana Demyanenko
Biomedicines 2022, 10(10), 2655; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10102655 - 20 Oct 2022
Cited by 1 | Viewed by 2081
Abstract
Our studies reveal changes in the expression of the main participants in the processing of amyloid precursor protein (APP) in neurons and astrocytes after photothrombotic stroke (PTS). Here we show the increase in the level of N- and C-terminal fragments of APP in [...] Read more.
Our studies reveal changes in the expression of the main participants in the processing of amyloid precursor protein (APP) in neurons and astrocytes after photothrombotic stroke (PTS). Here we show the increase in the level of N- and C-terminal fragments of APP in the cytoplasm of ischemic penumbra cells at 24 h after PTS and their co-immunoprecipitation with caveolin-1. The ADAM10 α-secretase level decreased in the rat brain cortex on the first day after PTS. Levels of γ-secretase complex proteins presenilin-1 and nicastrin were increased in astrocytes, but not in neurons, in the penumbra after PTS. Inhibitory analysis showed that these changes lead to neuronal death and activation of astrocytes in the early recovery period after PTS. The caveolin-1 inhibitor daidzein shifted APP processing towards Aβ synthesis, which caused astroglial activation. γ-secretase inhibitor DAPT down-regulated glial fibrillary acidic protein (GFAP) in astrocytes, prevented mouse cerebral cortex cells from PTS-induced apoptosis, and reduced the infarction volume. Thus, new generation γ-secretase inhibitors may be considered as potential agents for the treatment of stroke. Full article
(This article belongs to the Special Issue Brain Injury and Neurodegeneration: Molecular, Functional, and Translational Approach 2.0)
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13 pages, 783 KiB  
Article
Fatty Acid Levels and Their Inflammatory Metabolites Are Associated with the Nondipping Status and Risk of Obstructive Sleep Apnea Syndrome in Stroke Patients
by Arleta Drozd, Dariusz Kotlęga, Przemysław Nowacki, Sylwester Ciećwież, Tomasz Trochanowski and Małgorzata Szczuko
Biomedicines 2022, 10(9), 2200; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10092200 - 06 Sep 2022
Cited by 2 | Viewed by 1772
Abstract
Background: This paper discusses the role of inflammation in the pathogenesis of nondipping blood pressure and its role in the pathogenesis of obstructive sleep apnea syndrome. The aim of the study was to assess the impact of free fatty acids (FAs) and their [...] Read more.
Background: This paper discusses the role of inflammation in the pathogenesis of nondipping blood pressure and its role in the pathogenesis of obstructive sleep apnea syndrome. The aim of the study was to assess the impact of free fatty acids (FAs) and their inflammatory metabolites on the nondipping phenomenon and the risk of sleep apnea in stroke patients. Methods: Sixty-four ischemic stroke patients were included in the prospective study. Group I consisted of 33 patients with a preserved physiological dipping effect (DIP), while group II included 31 patients with the nondipping phenomenon (NDIP). All subjects had FA gas chromatography and inflammatory metabolite measurements performed with the use of liquid chromatography, their 24 h blood pressure was recorded, and they were assessed with the Epworth sleepiness scale (ESS). Results: In the nondipping group a higher level of C16:0 palmitic acid was observed, while lower levels were observed in regard to C20:0 arachidic acid, C22:0 behenic acid and C24:1 nervonic acid. A decreased leukotriene B4 level was recorded in the nondipping group. None of the FAs and derivatives correlated with the ESS scale in the group of patients after stroke. Correlations were observed after dividing into the DIP and NDIP groups. In the DIP group, a higher score of ESS was correlated with numerous FAs and derivatives. Inflammation of a lower degree and a higher level of anti-inflammatory mediators from EPA and DHA acids favored the occurrence of the DIP. A high level of C18: 3n6 gamma linoleic acid indicating advanced inflammation, intensified the NDIP effect. Conclusions: We demonstrated potential novel associations between the FA levels and eicosanoids in the pathogenesis of the nondipping phenomenon. There are common connections between fatty acids, their metabolites, inflammation, obstructive sleep apnea syndrome and nondipping in stroke patients. Full article
(This article belongs to the Special Issue Brain Injury and Neurodegeneration: Molecular, Functional, and Translational Approach 2.0)
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25 pages, 9304 KiB  
Article
Alcohol-Induced Alterations in the Vascular Basement Membrane in the Substantia Nigra of the Adult Human Brain
by Sandra Skuja, Nityanand Jain, Marks Smirnovs and Modra Murovska
Biomedicines 2022, 10(4), 830; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10040830 - 01 Apr 2022
Cited by 1 | Viewed by 2090
Abstract
The blood–brain barrier (BBB) represents a highly specialized interface that acts as the first line of defense against toxins. Herein, we investigated the structural and ultrastructural changes in the basement membrane (BM), which is responsible for maintaining the integrity of the BBB, in [...] Read more.
The blood–brain barrier (BBB) represents a highly specialized interface that acts as the first line of defense against toxins. Herein, we investigated the structural and ultrastructural changes in the basement membrane (BM), which is responsible for maintaining the integrity of the BBB, in the context of chronic alcoholism. Human post-mortem tissues from the Substantia Nigra (SN) region were obtained from 44 individuals, then grouped into controls, age-matched alcoholics, and non-age-matched alcoholics and assessed using light and electron microscopy. We found significantly less CD31+ vessels in alcoholic groups compared to controls in both gray and white matter samples. Alcoholics showed increased expression levels of collagen-IV, laminin-111, and fibronectin, which were coupled with a loss of BM integrity in comparison with controls. The BM of the gray matter was found to be more disintegrated than the white matter in alcoholics, as demonstrated by the expression of both collagen-IV and laminin-111, thereby indicating a breakdown in the BM’s structural composition. Furthermore, we observed that the expression of fibronectin was upregulated in the BM of the white matter vasculature in both alcoholic groups compared to controls. Taken together, our findings highlight some sort of aggregation or clumping of BM proteins that occurs in response to chronic alcohol consumption. Full article
(This article belongs to the Special Issue Brain Injury and Neurodegeneration: Molecular, Functional, and Translational Approach 2.0)
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8 pages, 3027 KiB  
Communication
NLRP3 Inhibition Reduces rt-PA Induced Endothelial Dysfunction under Ischemic Conditions
by Maximilian Bellut, Anthony T. Raimondi, Axel Haarmann, Lena Zimmermann, Guido Stoll and Michael K. Schuhmann
Biomedicines 2022, 10(4), 762; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10040762 - 24 Mar 2022
Cited by 3 | Viewed by 1790
Abstract
Thrombolysis with recombinant tissue plasminogen activator (rt-PA) is a mainstay of acute ischemic stroke treatment but is associated with bleeding complications, especially after prolonged large vessel occlusion. Recently, inhibition of the NLRP3 inflammasome led to preserved blood–brain barrier (BBB) integrity in experimental stroke [...] Read more.
Thrombolysis with recombinant tissue plasminogen activator (rt-PA) is a mainstay of acute ischemic stroke treatment but is associated with bleeding complications, especially after prolonged large vessel occlusion. Recently, inhibition of the NLRP3 inflammasome led to preserved blood–brain barrier (BBB) integrity in experimental stroke in vivo. To further address the potential of NLRP3 inflammasome inhibition as adjunct stroke treatment we used immortalized brain derived endothelial cells (bEnd5) as an in vitro model of the BBB. We treated bEnd5 with rt-PA in combination with the NLRP3 specific inhibitor MCC950 or vehicle under normoxic as well as ischemic (OGD) conditions. We found that rt-PA exerted a cytotoxic effect on bEnd5 cells under OGD confirming that rt-PA is harmful to the BBB. This detrimental effect could be significantly reduced by MCC950 treatment. Moreover, under ischemic conditions, the Cell Index—a sensible indicator for a patent BBB—and the protein expression of Zonula occludens 1 stabilized after MCC950 treatment. At the same time, the extent of endothelial cell death and NLRP3 expression decreased. In conclusion, NLRP3 inhibition can protect the BBB from rt-PA-induced damage and thereby potentially increase the narrow time window for safe thrombolysis in stroke. Full article
(This article belongs to the Special Issue Brain Injury and Neurodegeneration: Molecular, Functional, and Translational Approach 2.0)
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11 pages, 519 KiB  
Article
A Pilot Study of Whole-Blood Transcriptomic Analysis to Identify Genes Associated with Repetitive Low-Level Blast Exposure in Career Breachers
by Rany Vorn, Katie A. Edwards, James Hentig, Sijung Yun, Hyung-Suk Kim, Chen Lai, Christina Devoto, Angela M. Yarnell, Elena Polejaeva, Kristine C. Dell, Matthew L. LoPresti, Peter Walker, Walter Carr, James R. Stone, Stephen T. Ahlers and Jessica M. Gill
Biomedicines 2022, 10(3), 690; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10030690 - 17 Mar 2022
Cited by 5 | Viewed by 2650
Abstract
Repetitive low-level blast exposure is one of the major occupational health concerns among US military service members and law enforcement. This study seeks to identify gene expression using microRNA and RNA sequencing in whole-blood samples from experienced breachers and unexposed controls. We performed [...] Read more.
Repetitive low-level blast exposure is one of the major occupational health concerns among US military service members and law enforcement. This study seeks to identify gene expression using microRNA and RNA sequencing in whole-blood samples from experienced breachers and unexposed controls. We performed experimental RNA sequencing using Illumina’s HiSeq 2500 Sequencing System, and microRNA analysis using NanoString Technology nCounter miRNA expression panel in whole-blood total RNA samples from 15 experienced breachers and 14 age-, sex-, and race-matched unexposed controls. We identified 10 significantly dysregulated genes between experienced breachers and unexposed controls, with FDR corrected <0.05: One upregulated gene, LINC00996 (long intergenic non-protein coding RNA 996); and nine downregulated genes, IGLV3-16 (immunoglobulin lambda variable 3-16), CD200 (CD200 molecule), LILRB5 (leukocyte immunoglobulin-like receptor B5), ZNF667-AS1 (ZNF667 antisense RNA 1), LMOD1 (leiomodin 1), CNTNAP2 (contactin-associated protein 2), EVPL (envoplakin), DPF3 (double PHD fingers 3), and IGHV4-34 (immunoglobulin heavy variable 4-34). The dysregulated gene expressions reported here have been associated with chronic inflammation and immune response, suggesting that these pathways may relate to the risk of lasting neurological symptoms following high exposures to blast over a career. Full article
(This article belongs to the Special Issue Brain Injury and Neurodegeneration: Molecular, Functional, and Translational Approach 2.0)
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Review

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17 pages, 570 KiB  
Review
Neuropsychological Assessment in Patients with Traumatic Brain Injury: A Comprehensive Review with Clinical Recommendations
by William Torregrossa, Michele Torrisi, Rosaria De Luca, Carmela Casella, Carmela Rifici, Mirjam Bonanno and Rocco Salvatore Calabrò
Biomedicines 2023, 11(7), 1991; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines11071991 - 14 Jul 2023
Cited by 1 | Viewed by 3656
Abstract
Traumatic brain injury is damage to the brain occurring after birth, often resulting in the deterioration of cognitive, behavioural, and emotional functions. Neuropsychological evaluation can assist clinicians to better assess the patient’s clinical condition, reach differential diagnoses, and develop interventional strategies. However, considering [...] Read more.
Traumatic brain injury is damage to the brain occurring after birth, often resulting in the deterioration of cognitive, behavioural, and emotional functions. Neuropsychological evaluation can assist clinicians to better assess the patient’s clinical condition, reach differential diagnoses, and develop interventional strategies. However, considering the multiple rating scales available, it is not easy to establish which tool is most suitable for the different brain injury conditions. The aim of this review is to investigate and describe the most used neurocognitive assessment tools in patients with traumatic brain injury to provide clinicians with clear indications on their use in clinical practice. Indeed, during the acute phase, after the head trauma, alertness and wakefulness of the patients affected by a disorder of consciousness can be assessed using different scales, such as the Coma Recovery Scale-Revised. In both postacute and chronic phases after traumatic brain injury, general cognitive assessment tools (such as the Mini Mental State Examination) or more specific cognitive tests (e.g., Wisconsin Card Sorting Test and Trail Making Test) could be administered according to the patient’s functional status. In this way, clinicians may be aware of the patient’s neuropsychological and cognitive level, so they can guarantee a personalized and tailored rehabilitation approach in this frail patient population. Full article
(This article belongs to the Special Issue Brain Injury and Neurodegeneration: Molecular, Functional, and Translational Approach 2.0)
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18 pages, 374 KiB  
Review
Behavioral and Psychiatric Symptoms in Patients with Severe Traumatic Brain Injury: A Comprehensive Overview
by William Torregrossa, Loredana Raciti, Carmela Rifici, Giuseppina Rizzo, Gianfranco Raciti, Carmela Casella, Antonino Naro and Rocco Salvatore Calabrò
Biomedicines 2023, 11(5), 1449; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines11051449 - 15 May 2023
Cited by 4 | Viewed by 2761
Abstract
Traumatic brain injury (TBI) is defined as an altered brain structure or function produced by an external force. Adults surviving moderate and severe TBI often experience long-lasting neuropsychological and neuropsychiatric disorders (NPS). NPS can occur as primary psychiatric complications or could be an [...] Read more.
Traumatic brain injury (TBI) is defined as an altered brain structure or function produced by an external force. Adults surviving moderate and severe TBI often experience long-lasting neuropsychological and neuropsychiatric disorders (NPS). NPS can occur as primary psychiatric complications or could be an exacerbation of pre-existing compensated conditions. It has been shown that changes in behavior following moderate to severe TBI have a prevalence rate of 25–88%, depending on the methodology used by the different studies. Most of current literature has found that cognitive behavioral and emotional deficit following TBI occurs within the first six months whereas after 1–2 years the condition becomes stable. Identifying the risk factors for poor outcome is the first step to reduce the sequelae. Patients with TBI have an adjusted relative risk of developing any NPS several-fold higher than in the general population after six months of moderate–severe TBI. All NPS features of an individual’s life, including social, working, and familiar relationships, may be affected by the injury, with negative consequences on quality of life. This overview aims to investigate the most frequent psychiatric, behavioral, and emotional symptoms in patients suffering from TBI as to improve the clinical practice and tailor a more specific rehabilitation training. Full article
(This article belongs to the Special Issue Brain Injury and Neurodegeneration: Molecular, Functional, and Translational Approach 2.0)
31 pages, 2271 KiB  
Review
Understanding Acquired Brain Injury: A Review
by Liam Goldman, Ehraz Mehmood Siddiqui, Andleeb Khan, Sadaf Jahan, Muneeb U Rehman, Sidharth Mehan, Rajat Sharma, Stepan Budkin, Shashi Nandar Kumar, Ankita Sahu, Manish Kumar and Kumar Vaibhav
Biomedicines 2022, 10(9), 2167; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10092167 - 02 Sep 2022
Cited by 20 | Viewed by 5107
Abstract
Any type of brain injury that transpires post-birth is referred to as Acquired Brain Injury (ABI). In general, ABI does not result from congenital disorders, degenerative diseases, or by brain trauma at birth. Although the human brain is protected from the external world [...] Read more.
Any type of brain injury that transpires post-birth is referred to as Acquired Brain Injury (ABI). In general, ABI does not result from congenital disorders, degenerative diseases, or by brain trauma at birth. Although the human brain is protected from the external world by layers of tissues and bone, floating in nutrient-rich cerebrospinal fluid (CSF); it remains susceptible to harm and impairment. Brain damage resulting from ABI leads to changes in the normal neuronal tissue activity and/or structure in one or multiple areas of the brain, which can often affect normal brain functions. Impairment sustained from an ABI can last anywhere from days to a lifetime depending on the severity of the injury; however, many patients face trouble integrating themselves back into the community due to possible psychological and physiological outcomes. In this review, we discuss ABI pathologies, their types, and cellular mechanisms and summarize the therapeutic approaches for a better understanding of the subject and to create awareness among the public. Full article
(This article belongs to the Special Issue Brain Injury and Neurodegeneration: Molecular, Functional, and Translational Approach 2.0)
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38 pages, 953 KiB  
Review
TGF-β as a Key Modulator of Astrocyte Reactivity: Disease Relevance and Therapeutic Implications
by Jian Luo
Biomedicines 2022, 10(5), 1206; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10051206 - 23 May 2022
Cited by 18 | Viewed by 4849
Abstract
Astrocytes are essential for normal brain development and functioning. They respond to brain injury and disease through a process referred to as reactive astrogliosis, where the reactivity is highly heterogenous and context-dependent. Reactive astrocytes are active contributors to brain pathology and can exert [...] Read more.
Astrocytes are essential for normal brain development and functioning. They respond to brain injury and disease through a process referred to as reactive astrogliosis, where the reactivity is highly heterogenous and context-dependent. Reactive astrocytes are active contributors to brain pathology and can exert beneficial, detrimental, or mixed effects following brain insults. Transforming growth factor-β (TGF-β) has been identified as one of the key factors regulating astrocyte reactivity. The genetic and pharmacological manipulation of the TGF-β signaling pathway in animal models of central nervous system (CNS) injury and disease alters pathological and functional outcomes. This review aims to provide recent understanding regarding astrocyte reactivity and TGF-β signaling in brain injury, aging, and neurodegeneration. Further, it explores how TGF-β signaling modulates astrocyte reactivity and function in the context of CNS disease and injury. Full article
(This article belongs to the Special Issue Brain Injury and Neurodegeneration: Molecular, Functional, and Translational Approach 2.0)
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19 pages, 2333 KiB  
Review
Brain Trauma, Glucocorticoids and Neuroinflammation: Dangerous Liaisons for the Hippocampus
by Ilia G. Komoltsev and Natalia V. Gulyaeva
Biomedicines 2022, 10(5), 1139; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10051139 - 15 May 2022
Cited by 11 | Viewed by 4159
Abstract
Glucocorticoid-dependent mechanisms of inflammation-mediated distant hippocampal damage are discussed with a focus on the consequences of traumatic brain injury. The effects of glucocorticoids on specific neuronal populations in the hippocampus depend on their concentration, duration of exposure and cell type. Previous stress and [...] Read more.
Glucocorticoid-dependent mechanisms of inflammation-mediated distant hippocampal damage are discussed with a focus on the consequences of traumatic brain injury. The effects of glucocorticoids on specific neuronal populations in the hippocampus depend on their concentration, duration of exposure and cell type. Previous stress and elevated level of glucocorticoids prior to pro-inflammatory impact, as well as long-term though moderate elevation of glucocorticoids, may inflate pro-inflammatory effects. Glucocorticoid-mediated long-lasting neuronal circuit changes in the hippocampus after brain trauma are involved in late post-traumatic pathology development, such as epilepsy, depression and cognitive impairment. Complex and diverse actions of the hypothalamic–pituitary–adrenal axis on neuroinflammation may be essential for late post-traumatic pathology. These mechanisms are applicable to remote hippocampal damage occurring after other types of focal brain damage (stroke, epilepsy) or central nervous system diseases without obvious focal injury. Thus, the liaisons of excessive glucocorticoids/dysfunctional hypothalamic–pituitary–adrenal axis with neuroinflammation, dangerous to the hippocampus, may be crucial to distant hippocampal damage in many brain diseases. Taking into account that the hippocampus controls both the cognitive functions and the emotional state, further research on potential links between glucocorticoid signaling and inflammatory processes in the brain and respective mechanisms is vital. Full article
(This article belongs to the Special Issue Brain Injury and Neurodegeneration: Molecular, Functional, and Translational Approach 2.0)
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Jump to: Research, Review

19 pages, 966 KiB  
Systematic Review
Oral Microbiota, Its Equilibrium and Implications in the Pathophysiology of Human Diseases: A Systematic Review
by Barbara Giordano-Kelhoffer, Cristina Lorca, Jaume March Llanes, Alberto Rábano, Teodoro del Ser, Aida Serra and Xavier Gallart-Palau
Biomedicines 2022, 10(8), 1803; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10081803 - 27 Jul 2022
Cited by 10 | Viewed by 4377
Abstract
Imbalances of the oral microbiota and dysbiosis have traditionally been linked to the occurrence of teeth and oral diseases. However, recent findings indicate that this microbiota exerts relevant influence in systemic health. Dysbiosis of the oral microbiota is implicated in the apparition and [...] Read more.
Imbalances of the oral microbiota and dysbiosis have traditionally been linked to the occurrence of teeth and oral diseases. However, recent findings indicate that this microbiota exerts relevant influence in systemic health. Dysbiosis of the oral microbiota is implicated in the apparition and progression of cardiovascular, neurodegenerative and other major human diseases. In fact, the oral microbiota are the second most diverse and largely populated microbiota of the human body and its relationships with systemic health, although widely explored, they still lack of proper integration. The purpose of this systematic review is thus to widely examine the implications of oral microbiota in oral, cardiovascular and neurodegenerative diseases to offer integrative and up-to-date interpretations. To achieve that aim, we identified a total of 121 studies curated in PUBMED from the time interval January 2003–April 2022, which after careful screening resulted in 79 studies included. The reviewed scientific literature provides plausible vias of implication of dysbiotic oral microbiota in systemic human diseases, and encourages further research to continue elucidating the highly relevant and still poorly understood implications of this niche microbiota in systemic health. PROSPERO Registration Number: CRD42022299692. This systematic review follows relevant PRISMA guidelines. Full article
(This article belongs to the Special Issue Brain Injury and Neurodegeneration: Molecular, Functional, and Translational Approach 2.0)
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