Intercellular Adhesion Molecule-1-Induced Posttraumatic Brain Injury Neuropathology in the Prefrontal Cortex and Hippocampus Leads to Sensorimotor Function Deficits and Psychological Stress

Bhowmick, Saurav; Anitha, M.; Caruso, Danielle; Ponery, Nizmi; D’Mello, Veera; Finn, Christina; Abdul-Muneer, P. M.

doi:10.1523/eneuro.0242-21.2021

Cited by 14 publications

(8 citation statements)

References 76 publications

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“…A full systematic review has not been performed on pre-clinical studies of anxiety-related behaviors following TBI [but see (Semple et al, 2019) for an excellent summary]. The most consistency is with the FPI model, where increased anxiety-like behaviors are observed in most studies in both rats (Das et al, 2019;Dobrachinski et al, 2019;Fucich et al, 2019;Beitchman et al, 2020;Lapinlampi et al, 2020;Barretto et al, 2021) and mice (Tan et al, 2020;Tapp et al, 2020;Bhowmick et al, 2021), although in some studies this result is dependent on the time testing took place after injury. There is limited evidence from some CCI studies that results and conclusions from anxiety testing may depend on the time after injury at which behavioral testing takes place, or on the specific behavioral test employed Popovitz et al, 2019).…”

Section: Anxiety-like Symptoms Post-tbi In Rodentsmentioning

confidence: 99%

Measuring Anxiety-Like Behaviors in Rodent Models of Traumatic Brain Injury

Tucker

McCabe

2021

Front. Behav. Neurosci.

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Anxiety is a common complaint following acquired traumatic brain injury (TBI). However, the measurement of dysfunctional anxiety behavioral states following experimental TBI in rodents is complex. Some studies report increased anxiety after TBI, whereas others find a decreased anxiety-like state, often described as increased risk-taking behavior or impulsivity. These inconsistencies may reflect a lack of standardization of experimental injury models or of behavioral testing techniques. Here, we review the most commonly employed unconditioned tests of anxiety and discuss them in a context of experimental TBI. Special attention is given to the effects of repeated testing, and consideration of potential sensory and motor confounds in injured rodents. The use of multiple tests and alternative data analysis methods are discussed, as well as the potential for the application of common data elements (CDEs) as a means of providing a format for documentation of experimental details and procedures of each published research report. CDEs may improve the rigor, reproducibility, as well as endpoint for better relating findings with clinical TBI phenotypes and the final goal of translation. While this may not resolve all incongruities in findings across laboratories, it is seen as a way forward for standardized and universal data collection for improvement of data quality and sharing, and advance therapies for neuropsychiatric symptoms that often present for decades following TBI.

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Section: Anxiety-like Symptoms Post-tbi In Rodentsmentioning

confidence: 99%

Measuring Anxiety-Like Behaviors in Rodent Models of Traumatic Brain Injury

Tucker

McCabe

2021

Front. Behav. Neurosci.

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“… 22 The results of this study showed that the level of ICAM-1 was higher in patients with HICH, and the higher the degree of brain injury, the higher the level of ICAM-1 expression, suggesting that ICAM-1 is associated with HICH, which basically in line with the post-hoc analysis by Witsch et al 23 Meanwhile, ICAM-1 is a risk factor affecting the poor prognosis of patients with HICH. Bhowmick S et al 24 have shown that the neural complications caused by traumatic brain injury can be treated by blocking the activation of ICAM-1, so as to reduce the migration of immune cells to the brain, neuroinflammation, and cell death, confirming that ICAM-1 levels correlate with the severity of patients with brain injury. The animal experiments by Abadier M et al 25 showed that the ICAM-1 level of endothelial cells is the most critical factor to guide cd4+ TEM cells to move through the blood-brain barrier.…”

Section: Discussionmentioning

confidence: 92%

Clinical changes of serum melatonin and ICAM-1 levels in patients with basal ganglia hypertensive intracerebral hemorrhage

Hou¹,

2023

Pak J Med Sci

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Objective: To investigate the clinical changes of serum melatonin and intercellular adhesion molecule-1 (ICAM-1) levels in patients with basal ganglia hypertensive intracerebral hemorrhage (HICH). Methods: In this retrospective observational study, patients with HICH in Suzhou Hospital of Traditional Chinese and Western Medicine from January 2020 to January 2021 were included as the observation group (n=120), and 120 healthy volunteers who underwent physical examination were included as the control group. According to the Glasgow Coma Scale (GCS), the observation group was divided into four subgroups: normal group (n=27), mild group (n=51), moderate group (n=24), and severe group (n=18). Differences in serum melatonin and ICAM-1 were compared between the observation group and the control group, and between the subgroups. Logistic regression was used to analyze the risk factors of poor prognosis, and the ROC curve was used to analyze the influence of melatonin and ICAM-1 levels on patient prognosis. Results: Serum melatonin levels were lower in the observation group compared to the control group, while ICAM-1 levels were higher (P<0.05). With the aggravation of brain injury, serum melatonin decreased and ICAM increased (P<0.05). Decreased serum melatonin and increased ICAM-1 were independent risk factors for poor prognosis in patients with HICH. The combined AUC of serum melatonin and ICAM-1 for the detection of poor prognosis in patients with HICH was 0.860, which was higher than that of the two alone (P<0.05). Conclusions: Low serum melatonin levels and high ICAM-1 levels are associated with poor prognosis in patients with HICH and can be used as predictors of patients’ prognosis. doi: https://doi.org/10.12669/pjms.39.4.7252 How to cite this: Hou H, Li X. Clinical changes of serum melatonin and ICAM-1 levels in patients with basal ganglia hypertensive intracerebral hemorrhage. Pak J Med Sci. 2023;39(4):---------. doi: https://doi.org/10.12669/pjms.39.4.7252 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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“…A strong correlation exists between traumatic brain injury-mediated inflammation and impairment in functional outcomes following brain trauma and concentration of ICAM-1. On the other hand, the deletion or blocking of ICAM-1 resulted in a better outcome in attenuating neuroinflammation [ 47 ]. It is interesting that adapted WSN and NS80 viruses induced lower levels of ICAM-1 and are less pathogenic than WSN virus.…”

Section: Discussionmentioning

confidence: 99%

Changes in the Expression of Proteins Associated with Neurodegeneration in the Brains of Mice after Infection with Influenza A Virus with Wild Type and Truncated NS1

Donátová,

Mladá,

Lopušná

et al. 2024

IJMS

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Influenza type A virus (IAV) infection is a major cause of morbidity and mortality during influenza epidemics. Recently, a specific link between IAV infection and neurodegenerative disease progression has been established. The non-structural NS1 protein of IAV regulates viral replication during infection and antagonizes host antiviral responses, contributing to influenza virulence. In the present study, we have prepared a mouse lung-to-lung adapted to the NS1-truncated virus (NS80ad). Transcriptome analysis of the gene expression in the lungs revealed that infection with wild-type A/WSN/33 (WSN), NS80, and NS80ad viruses resulted in different regulation of genes involved in signaling pathways associated with the cell proliferation, inflammatory response, and development of neurodegenerative diseases. NS1 protein did not influence the genes involved in the RIG-I-like receptor signaling pathway in the brains. Lethal infection with IAVs dysregulated expression of proteins associated with the development of neurodegenerative diseases (CX3CL1/Fractalkine, Coagulation factor III, and CD105/Endoglin, CD54/ICAM-1, insulin-like growth factor-binding protein (IGFBP)-2, IGFBP-5, IGFBP-6, chitinase 3-like 1 (CHI3L1), Myeloperoxidase (MPO), Osteopontin (OPN), cystatin C, and LDL R). Transcription of GATA3 mRNA was decreased, and expression of MPO was inhibited in the brain infected with NS80 and NS80ad viruses. In addition, the truncation of NS1 protein led to reduced expression of IGFBP-2, CHI3L1, MPO, and LDL-R proteins in the brains. Our results indicate that the influenza virus influences the expression of proteins involved in brain function, and this might occur mostly through the NS1 protein. These findings suggest that the abovementioned proteins represent a promising target for the development of potentially effective immunotherapy against neurodegeneration.

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Intercellular Adhesion Molecule-1-Induced Posttraumatic Brain Injury Neuropathology in the Prefrontal Cortex and Hippocampus Leads to Sensorimotor Function Deficits and Psychological Stress

Cited by 14 publications

References 76 publications

Measuring Anxiety-Like Behaviors in Rodent Models of Traumatic Brain Injury

Measuring Anxiety-Like Behaviors in Rodent Models of Traumatic Brain Injury

Clinical changes of serum melatonin and ICAM-1 levels in patients with basal ganglia hypertensive intracerebral hemorrhage

Changes in the Expression of Proteins Associated with Neurodegeneration in the Brains of Mice after Infection with Influenza A Virus with Wild Type and Truncated NS1

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