Brain Injury and Neurodegeneration: Molecular, Functional, and Translational Approach 3.0

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

Deadline for manuscript submissions: 30 June 2024 | Viewed by 3500

Special Issue Editors


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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
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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

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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

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

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 Special 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 Special 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. Meenakshi Ahluwalia
Dr. Pankaj Gaur
Dr. Pankaj 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

Published Papers (3 papers)

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Research

14 pages, 2046 KiB  
Article
Hyperchloremia and Hypernatremia Decreased Microglial and Neuronal Survival during Oxygen–Glucose Deprivation/Reperfusion
by Reetika Mahajan, Faheem Shehjar, Adnan I. Qureshi and Zahoor A. Shah
Biomedicines 2024, 12(3), 551; https://doi.org/10.3390/biomedicines12030551 - 29 Feb 2024
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Abstract
Hyperchloremia and hypernatremia are associated with higher mortality in ischemic stroke, but it remains unclear whether their influence directly contributes to ischemic injury. We investigated the impact of 0.9% sodium chloride (154 mM NaCl), 0.9% sodium acetate (167 mM CH3COONa), and [...] Read more.
Hyperchloremia and hypernatremia are associated with higher mortality in ischemic stroke, but it remains unclear whether their influence directly contributes to ischemic injury. We investigated the impact of 0.9% sodium chloride (154 mM NaCl), 0.9% sodium acetate (167 mM CH3COONa), and their different combinations (3:1, 2:1, and 1:1) on microglial (HMC-3) and neuronal (differentiated SH-SY5Y) survival during oxygen–glucose deprivation/reperfusion (OGD/R). Further, we assessed the effect of hyperchloremia and hypernatremia-treated and OGD/R-induced HMC-3-conditioned media on differentiated SH-SY5Y cells under OGD/R conditions. We performed cell viability, cell toxicity, and nitric oxide (NO) release assays and studied the alteration in expression of caspase-1 and caspase-3 in different cell lines when exposed to hyperchloremia and hypernatremia. Cell survival was decreased in 0.9% NaCl, 0.9% CH3COONa, combinations of HMC-3 and differentiated SH-SY5Y, and differentiated SH-SY5Y cells challenged with HMC-3-conditioned media under normal and OGD/R conditions. Under OGD/R conditions, differentiated SH-SY5Y cells were less likely to survive exposure to 0.9% NaCl. Expression of caspase-1 and caspase-3 in HMC-3 and differentiated SH-SY5Y cells was altered when exposed to 0.9% NaCl, 0.9% CH3COONa, and their combinations. A total of 0.9% NaCl and 0.9% CH3COONa and their combinations decreased the NO production in HMC-3 cells under normal and OGD/R conditions. Both hypernatremia and hyperchloremia reduced the survival of HMC-3 and differentiated SH-SY5Y cells under OGD/R conditions. Based on the OGD/R in vitro model that mimics human ischemic stroke conditions, it possibly provides a link for the increased death associated with hyperchloremia or hypernatremia in stroke patients. Full article
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16 pages, 1767 KiB  
Article
Association between Serum GDF-15 and Cognitive Dysfunction in Hemodialysis Patients
by Hae Ri Kim, Moo Jun Kim, Jae Wan Jeon, Young Rok Ham, Ki Ryang Na, Hyerim Park, Jwa-Jin Kim and Dae Eun Choi
Biomedicines 2024, 12(2), 358; https://doi.org/10.3390/biomedicines12020358 - 3 Feb 2024
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Abstract
Cognitive dysfunction is more frequent in end-stage renal disease (ESRD) patients undergoing hemodialysis compared with the healthy population, emphasizing the need for early detection. Interest in serum markers that reflect cognitive function has recently increased. Elevated serum growth differentiation factor 15 (GDF-15) levels [...] Read more.
Cognitive dysfunction is more frequent in end-stage renal disease (ESRD) patients undergoing hemodialysis compared with the healthy population, emphasizing the need for early detection. Interest in serum markers that reflect cognitive function has recently increased. Elevated serum growth differentiation factor 15 (GDF-15) levels are known to be associated with an increased risk of decreased renal function and cognitive dysfunction. This study investigated the relationship between GDF-15 and cognitive dysfunction in hemodialysis patients using a retrospective analysis of 92 individuals aged ≥ 18 years. Cognitive function was assessed using the Korean version of the Mini-Mental Status Examination (K-MMSE), categorizing patients into normal (≥24 points) and cognitive dysfunction (<24 points). As a result, serum GDF-15 concentrations were at significantly higher levels in the cognitive dysfunction group (7500.42 pg/mL, p = 0.001). Logistic regression indicated an increased risk of K-MMSE scores < 24 points when serum GDF-15 exceeded 5408.33 pg/mL. After indoxyl sulfate exposure in HT22 cells, HT22 cells survival was decreased and GDF-15 expression in HT22 cells was increased. Similarly, exposure to indoxyl sulfate in mouse brain tissue resulted in an increased expression of GDF-15. This study highlights the potential of serum GDF-15 as a marker for cognitive dysfunction in hemodialysis patients, offering a valuable screening tool. Serum GDF-15 is related to cognitive dysfunction in hemodialysis patients and may be helpful in screening for cognitive dysfunction in hemodialysis patients. Full article
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20 pages, 10423 KiB  
Article
Next-Generation Proteomics of Brain Extracellular Vesicles in Schizophrenia Provide New Clues on the Altered Molecular Connectome
by Cristina Lorca, María Fernández-Rhodes, Jose Antonio Sánchez Milán, María Mulet, Félix Elortza, Alfredo Ramos-Miguel, Luis F. Callado, J. Javier Meana, Maria Mur, Iolanda Batalla, Elisabet Vilella, Aida Serra and Xavier Gallart-Palau
Biomedicines 2024, 12(1), 129; https://doi.org/10.3390/biomedicines12010129 - 8 Jan 2024
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Abstract
Extracellular vesicles (EVs) are tiny membranous structures that mediate intercellular communication. The role(s) of these vesicles have been widely investigated in the context of neurological diseases; however, their potential implications in the neuropathology subjacent to human psychiatric disorders remain mostly unknown. Here, by [...] Read more.
Extracellular vesicles (EVs) are tiny membranous structures that mediate intercellular communication. The role(s) of these vesicles have been widely investigated in the context of neurological diseases; however, their potential implications in the neuropathology subjacent to human psychiatric disorders remain mostly unknown. Here, by using next-generation discovery-driven proteomics, we investigate the potential role(s) of brain EVs (bEVs) in schizophrenia (SZ) by analyzing these vesicles from the three post-mortem anatomical brain regions: the prefrontal cortex (PFC), hippocampus (HC), and caudate (CAU). The results obtained indicate that bEVs from SZ-affected brains contain region-specific proteins that are associated with abnormal GABAergic and glutamatergic transmission. Similarly, these vesicles from the analyzed regions were implicated in synaptic decay, abnormal brain immunity, neuron structural imbalances, and impaired cell homeostasis. Our findings also provide evidence, for the first time, that networks of molecular exchange (involving the PFC, HC, and CAU) are potentially active and mediated by EVs in non-diseased brains. Additionally, these bEV-mediated networks seem to have become partially reversed and largely disrupted in the brains of subjects affected by SZ. Taken as a whole, these results open the door to the uncovering of new biological markers and therapeutic targets, based on the compositions of bEVs, for the benefit of patients affected by SZ and related psychotic disorders. Full article
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