Molecular Mechanisms in Brain Injury

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (30 September 2022) | Viewed by 2467

Special Issue Editors


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Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Messina, Italy
Interests: pathology; inflammation; brain injury; neurodegenerative disorders

Special Issue Information

Dear Colleagues,

There are two types of brain injury: traumatic brain injury and acquired brain injury. Both disrupt the brain’s normal functioning. “Traumatic Brain Injury” (TBI) is caused by an external force; on the other hand, “Acquired Brain Injury” (ABI) occurs at the cellular level and is most often associated with pressure on the brain (for example, from a tumor or a stroke). In both cases, the brain injury typically disturbs brain functions and leads to multiple behavioral and cognitive dysfunctions.

The aim of this Special Issue is to better understand the complicated molecular pathways involved in brain injury such as neuroinflammation, oxidative/nitrosative stress, and cytokine cascades; to investigate the physiological brain alterations in more depth; and, more importantly, to discover potential treatments to propose new therapeutic strategies for the management of TBI, ABI, or other brain injuries.

Dr. Marika Cordaro
Prof. Dr. Tiziana Genovese
Guest Editors

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Keywords

  • brain injury
  • inflammation
  • oxidative stress
  • new therapeutic target
  • behavioral alterations

Published Papers (1 paper)

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Research

21 pages, 3533 KiB  
Article
Phosphatidylethanolamine Deficiency and Triglyceride Overload in Perilesional Cortex Contribute to Non-Goal-Directed Hyperactivity after Traumatic Brain Injury in Mice
by Lisa Hahnefeld, Alexandra Vogel, Robert Gurke, Gerd Geisslinger, Michael K. E. Schäfer and Irmgard Tegeder
Biomedicines 2022, 10(4), 914; https://doi.org/10.3390/biomedicines10040914 - 15 Apr 2022
Cited by 6 | Viewed by 1922
Abstract
Traumatic brain injury (TBI) is often complicated by long-lasting disabilities, including headache, fatigue, insomnia, hyperactivity, and cognitive deficits. In a previous study in mice, we showed that persistent non-goal-directed hyperactivity is a characteristic post-TBI behavior that was associated with low levels of endocannabinoids [...] Read more.
Traumatic brain injury (TBI) is often complicated by long-lasting disabilities, including headache, fatigue, insomnia, hyperactivity, and cognitive deficits. In a previous study in mice, we showed that persistent non-goal-directed hyperactivity is a characteristic post-TBI behavior that was associated with low levels of endocannabinoids in the perilesional cortex. We now analyzed lipidome patterns in the brain and plasma in TBI versus sham mice in association with key behavioral parameters and endocannabinoids. Lipidome profiles in the plasma and subcortical ipsilateral and contralateral brain were astonishingly equal in sham and TBI mice, but the ipsilateral perilesional cortex revealed a strong increase in neutral lipids represented by 30 species of triacylglycerols (TGs) of different chain lengths and saturation. The accumulation of TG was localized predominantly to perilesional border cells as revealed by Oil Red O staining. In addition, hexosylceramides (HexCer) and phosphatidylethanolamines (PE and ether-linked PE-O) were reduced. They are precursors of gangliosides and endocannabinoids, respectively. High TG, low HexCer, and low PE/PE-O showed a linear association with non-goal-directed nighttime hyperactivity but not with the loss of avoidance memory. The analyses suggest that TG overload and HexCer and PE deficiencies contributed to behavioral dimensions of post-TBI psychopathology. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Brain Injury)
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