Demyelinating diseases as a result of cerebral edema?

Barz, Helmut; Schreiber, Almut; Barz, Ulrich

doi:10.1016/j.mehy.2017.05.010

Cited by 11 publications

(7 citation statements)

References 26 publications

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“…In addition, cerebral edema, as the most common pathological process following SAH, may also modulate demyelination by increasing local tissue pressure and stretching myelinated ber bundles, which is similar to the ndings of previous studies [37].…”

Section: Discussionsupporting

confidence: 89%

Dexras1 Induces Dysdifferentiation of Oligodendrocytes by Inhibiting the cAMP-CREB Pathway in White Matter Injury After Subarachnoid Hemorrhage

Xin¹,

Zhang²,

Chen³

et al. 2021

Preprint

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BackgroundWhite matter damage (WMD), different from the widely studied neuronal death, is also involved in neurological dysfunction after subarachnoid hemorrhage (SAH) although the specific mechanism is not yet known. Dexras1 (RASD1) has been reported to be involved in nervous system damage in autoimmune encephalitis and multiple sclerosis; however, there is no information on whether Dexras1 participates in WMD after SAH. We hypothesized that Dexras1 participates in oligodendrocyte precursor cell (OPC) differentiation in WMD after SAH.MethodsIntracerebroventricular lentiviral administration was used to modulate Dexras1 levels to determine its functional influence on neurological injuries after SAH. Immunofluorescence, transmission electron microscopy, and Western blotting were used to investigate the effects of Dexras1 on demyelination, glial cell activation and differentiation of OPCs after SAH. Primary rat brain neurons were treated with oxyhemoglobin to elucidate the association between Dexras1 and cAMP-CREB.ResultsDexras1 levels were significantly increased after SAH, accompanied by clear neurological deficits, glial cell activation, OPC differentiation disorders, and myelin injury. Dexras1 overexpression significantly worsened OPC dysdifferentiation and myelin injury after SAH, which were accompanied by increased glial cell activation and levels of inflammatory factors. In contrast, Dexras1 knockdown ameliorated demyelination, oligodendrocyte differentiation disorders, and glial cell activation. cAMP acted as an upstream agonist of CREB, with decreased TNF-α and IL-1β levels after SAH. However, the cAMP-CREB pathway was inhibited after Dexras1 overexpression.ConclusionDexras1 induced oligodendrocyte dysdifferentiation after SAH and regulated glial cell activation through suppression of the cAMP-CREB pathway. This research highlights a novel direction for the improvement of neurological dysfunction after SAH.

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Section: Discussionsupporting

confidence: 89%

Dexras1 Induces Dysdifferentiation of Oligodendrocytes by Inhibiting the cAMP-CREB Pathway in White Matter Injury After Subarachnoid Hemorrhage

Xin¹,

Zhang²,

Chen³

et al. 2021

Preprint

View full text Add to dashboard Cite

show abstract

“…A recent hypothesis proposes that cerebral edema can cause demyelination in certain regions of the brain [3]. The authors postulate that the increased pressure, leading to mechanical stress, and oxygen and glucose deprivation, can contribute to loss of myelin and parenchymal cells.…”

Section: Oligodendrocyte Precursor Cellsmentioning

confidence: 99%

Aneurysmal Subarachnoid Hemorrhage: an Overview of Inflammation-Induced Cellular Changes

Coulibaly

Provencio

2020

Neurotherapeutics

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Aneurysmal subarachnoid hemorrhage (SAH) is a devastating disease that leads to poor neurological outcomes and is characterized by both vascular and neural pathologies. Recent evidence demonstrates that inflammation mediates many of the vascular and neural changes observed after SAH. Although most studies focus on inflammatory mediators such as cytokines, the ultimate effectors of inflammation in SAH are parenchymal brain and peripheral immune cells. As such, the present review will summarize our current understanding of the cellular changes of both CNS parenchymal and peripheral immune cells after SAH.

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“…In addition, another remark of an ultrastructural change in the brain was myelin degeneration, highly presented in nontreated immunocompromised mice (Figure 7). A breakdown of myelin sheath is one of the causes of axonal degeneration, which closely reflects to brain oedema [34] and relates to the high intracranial pressure condition [35] and the release of proinflammatory cytokines, e.g., TNF- α [36]. In line with these evidences, brain oedema induced by S. apiospermum infection leads to myelin degeneration due to the cytokines from abscess, cerebral oedematous condition, and the increase of intracranial pressure from space-occupying mass.…”

Section: Discussionmentioning

confidence: 99%

Experimental Scedosporiosis Induces Cerebral Oedema Associated with Abscess regarding Aquaporin-4 and Nrf-2 Depletions

Ampawong

Luplertlop

2019

BioMed Research International

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Cerebral involvement especially brain abscess is life-threatening complication and major cause of death during Scedosporium apiospermum infection. However, little is known about pathogenesis of brain oedema associated with abscess in scedosporiosis. Experimental scedosporiosis was conducted in BALB/cMlac mice to characterize the presence of brain oedema, its type, and its related mechanisms focusing on aquaporin (AQP)-4, nuclear factor erythroid-2 related factor (Nrf-2), and tumor necrotic factor (TNF)-α. The results revealed that S. apiospermum infection induced severe inflammatory environment relevant to TNF-α expression and cytogenic oedema-associated brain abscess predominately in cerebrum of immunocompromised mice without voriconazole treatment reflecting to downregulation of AQP-4 in neighboring abscess areas and oedematous blood vessels. Downregulation of Nrf-2 in neuronal cells and myelin degeneration were significantly observed in nontreated mice. In summary, oxidative stress, severe inflammatory response, and space-occupying mass from abscess formation inducing tissue hypoxia might be the postulate causes of oedema induced by scedosporiosis.

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Demyelinating diseases as a result of cerebral edema?

Cited by 11 publications

References 26 publications

Dexras1 Induces Dysdifferentiation of Oligodendrocytes by Inhibiting the cAMP-CREB Pathway in White Matter Injury After Subarachnoid Hemorrhage

Dexras1 Induces Dysdifferentiation of Oligodendrocytes by Inhibiting the cAMP-CREB Pathway in White Matter Injury After Subarachnoid Hemorrhage

Aneurysmal Subarachnoid Hemorrhage: an Overview of Inflammation-Induced Cellular Changes

Experimental Scedosporiosis Induces Cerebral Oedema Associated with Abscess regarding Aquaporin-4 and Nrf-2 Depletions

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