TY  - JOUR
A1  - Schadt, Fabian
A1  - Israel, Ina
A1  - Beez, Alexandra
A1  - Alushi, Kastriot
A1  - Weiland, Judith
A1  - Ernestus, Ralf-Ingo
A1  - Westermaier, Thomas
A1  - Samnick, Samuel
A1  - Lilla, Nadine
T1  - Analysis of cerebral glucose metabolism following experimental subarachnoid hemorrhage over 7 days
JF  - Scientific Reports
N2  - Little is known about changes in brain metabolism following SAH, possibly leading towards secondary brain damage. Despite sustained progress in the last decade, analysis of in vivo acquired data still remains challenging. The present interdisciplinary study uses a semi-automated data analysis tool analyzing imaging data independently from the administrated radiotracer. The uptake of 2-[18F]Fluoro-2-deoxy-glucose ([\(^{18}\)F]FDG) was evaluated in different brain regions in 14 male Sprague–Dawley rats, randomized into two groups: (1) SAH induced by the endovascular filament model and (2) sham operated controls. Serial [\(^{18}\)F]FDG-PET measurements were carried out. Quantitative image analysis was performed by uptake ratio using a self-developed MRI-template based data analysis tool. SAH animals showed significantly higher [\(^{18}\)F]FDG accumulation in gray matter, neocortex and olfactory system as compared to animals of the sham group, while white matter and basal forebrain region showed significant reduced tracer accumulation in SAH animals. All significant metabolic changes were visualized from 3 h, over 24 h (day 1), day 4 and day 7 following SAH/sham operation. This [\(^{18}\)F]FDG-PET study provides important insights into glucose metabolism alterations following SAH—for the first time in different brain regions and up to day 7 during course of disease.
KW  - SAH
KW  - metabolism
KW  - brain
Y1  - 2023
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-300725
VL  - 13
IS  - 1
ER  - 
TY  - JOUR
A1  - Weiland, Judith
A1  - Beez, Alexandra
A1  - Westermaier, Thomas
A1  - Kunze, Ekkehard
A1  - Sirén, Anna-Leena
A1  - Lilla, Nadine
T1  - Neuroprotective strategies in aneurysmal subarachnoid hemorrhage (aSAH)
JF  - International Journal of Molecular Sciences
N2  - 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.
KW  - subarachnoid hemorrhage (SAH)
KW  - inflammation
KW  - thromboinflammation
KW  - metabolism
KW  - neuroprotection
KW  - therapy
Y1  - 2021
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-260755
SN  - 1422-0067
VL  - 22
IS  - 11
ER  -