Neuroprotective Strategies in Aneurysmal Subarachnoid Hemorrhage (aSAH)

Aneurysmal subarachnoid hemorrhage (aSAH) remains a disease with high mortality and morbidity. Since treating vasospasm has not inevitably led to an improvement in outcome, the actual emphasis is on finding neuroprotective therapies in the early phase following aSAH to prevent secondary brain injury...

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Bibliographic Details
Published in:International journal of molecular sciences 2021-05, Vol.22 (11), p.5442
Main Authors: Weiland, Judith, Beez, Alexandra, Westermaier, Thomas, Kunze, Ekkehard, Sirén, Anna-Leena, Lilla, Nadine
Format: Article
Language:English
Subjects:
Animals
Brain Injuries - metabolism
Cytokines - metabolism
Humans
inflammation
Inflammation - metabolism
metabolism
neuroprotection
Neuroprotection - physiology
Review
Signal Transduction - physiology
subarachnoid hemorrhage (SAH)
Subarachnoid Hemorrhage - metabolism
therapy
thromboinflammation
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Summary:Aneurysmal subarachnoid hemorrhage (aSAH) remains a disease with high mortality and morbidity. Since treating vasospasm has not inevitably led to an improvement in outcome, the actual emphasis is on finding neuroprotective therapies in the early phase following aSAH to prevent secondary brain injury in the later phase of disease. Within the early phase, neuroinflammation, thromboinflammation, disturbances in brain metabolism and early neuroprotective therapies directed against delayed cerebral ischemia (DCI) came into focus. Herein, the role of neuroinflammation, thromboinflammation and metabolism in aSAH is depicted. Potential neuroprotective strategies regarding neuroinflammation target microglia activation, metalloproteases, autophagy and the pathway via Toll-like receptor 4 (TLR4), high mobility group box 1 (HMGB1), NF-κB and finally the release of cytokines like TNFα or IL-1. Following the link to thromboinflammation, potential neuroprotective therapies try to target microthrombus formation, platelets and platelet receptors as well as clot clearance and immune cell infiltration. Potential neuroprotective strategies regarding metabolism try to re-balance the mismatch of energy need and supply following aSAH, for example, in restoring fuel to the TCA cycle or bypassing distinct energy pathways. Overall, this review addresses current neuroprotective strategies in aSAH, hopefully leading to future translational therapy options to prevent secondary brain injury.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms22115442