Atlas registration for edema-corrected MRI lesion volume in mouse stroke models

Koch, Stefan P.; Mueller, Susanne; Foddis, Marco; Bienert, Thomas; Elverfeldt, Dominik von; Knab, Felix; Farr, Tracy D.; Bernard, René; Dopatka, Monika; Rex, André; Dirnagl, Ulrich; Harms, Christoph; Boehm‐Sturm, Philipp

doi:10.1177/0271678x17726635

Cited by 53 publications

(69 citation statements)

References 38 publications

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“…The sections were photographed, and the resulting infarct areas were measured using ImageJ (the examples of the obtained images are presented on the website). Infarct sizes were presented as the hemispheric lesion volumes corrected for oedema (%HLVe) [24,25].…”

Section: Infarct Size Measurementmentioning

confidence: 99%

Neuroprotection in Rats Following Ischaemia-Reperfusion Injury by GLP-1 Analogues—Liraglutide and Semaglutide

Basalay

Davidson

Yellon

2019

Cardiovasc Drugs Ther

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Purpose A substantial number of ischaemic stroke patients who receive reperfusion therapy in the acute phase do not ever fully recover. This reveals the urgent need to develop new adjunctive neuroprotective treatment strategies alongside reperfusion therapy. Previous experimental studies demonstrated the potential of glucagon-like peptide-1 (GLP-1) to reduce acute ischaemic damage in the brain. Here, we examined the neuroprotective effects of two GLP-1 analogues, liraglutide and semaglutide. Methods A non-diabetic rat model of acute ischaemic stroke involved 90, 120 or 180 min of middle cerebral artery occlusion (MCAO). Liraglutide or semaglutide was administered either i.v. at the onset of reperfusion or s.c. 5 min before the onset of reperfusion. Infarct size and functional status were evaluated after 24 h or 72 h of reperfusion. Results Liraglutide, administered as a bolus at the onset of reperfusion, reduced infarct size by up to 90% and improved neuroscore at 24 h in a dose-dependent manner, following 90-min, but not 120-min or 180-min ischaemia. Semaglutide and liraglutide administered s.c. reduced infarct size by 63% and 48%, respectively, and improved neuroscore at 72 h following 90min MCAO. Neuroprotection by semaglutide was abolished by GLP1-R antagonist exendin(9-39). Conclusion Infarct-limiting and functional neuroprotective effects of liraglutide are dose-dependent. Neuroprotection by semaglutide is at least as strong as by liraglutide and is mediated by GLP-1Rs.

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Section: Infarct Size Measurementmentioning

confidence: 99%

Neuroprotection in Rats Following Ischaemia-Reperfusion Injury by GLP-1 Analogues—Liraglutide and Semaglutide

Basalay

Davidson

Yellon

2019

Cardiovasc Drugs Ther

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“…The stroke lesion will be segmented on T2w images 24 h post-surgery using Analyze 10.0 software (AnalyzeDirect, Overland Park, KS, USA) by selecting hyperintense areas of ischemic tissue by an experienced researcher and a mask will be exported. The 24 h lesion mask, and 21 d DTI parameter maps will coregistered to the Allen mouse brain atlas using their corresponding anatomical T2w images in the MATLAB toolbox ANTX ( https://github.com/philippboehmsturm/ANTX/ ) 23 – 25 . Since the registration includes nonlinear terms, lesion volumes are effectively corrected for edema when measured in atlas space.…”

Section: Methodsmentioning

confidence: 99%

Stage 1 Registered Report: Effect of deficient phagocytosis on neuronal survival and neurological outcome after temporary middle cerebral artery occlusion (tMCAo)

et al. 2018

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Stroke is a major cause of death and disability worldwide. In addition to neuronal death resulting directly from energy depletion due to lack of blood supply, inflammation and microglial activation following ischemic brain injury has been increasingly recognized to be a key contributor to the pathophysiology of cerebrovascular disease. However, our understanding of the cross talk between the ischemic brain and the immune system is limited. Recently, we demonstrated that following focal ischemia, death of mature viable neurons can be executed through phagocytosis by microglial cells or recruited macrophages, i.e. through phagoptosis. It was shown that inhibition of phagocytic signaling pathways following endothelin-1 induced focal cerebral ischemia leads to increased neuronal survival and neurological recovery. This suggests that inhibition of specific phagocytic pathways may prevent neuronal death during cerebral ischemia. To further explore this potential therapeutic target, we propose to assess the role of phagocytosis in an established model of temporary (45min) middle cerebral artery occlusion (tMCAo), and to evaluate neuronal survival and neurological recovery in mice with deficient phagocytosis. The primary outcome of this study will be forelimb function assessed with the staircase test. Secondary outcomes constitute Rotarod performance, stroke volume (quantified on MR imaging or brain sections, respectively), diffusion tensor imaging (DTI) connectome mapping, and histological analyses to measure neuronal and microglial densities, and phagocytic activity. Male mice aged 10-12 weeks will be used for experiments.

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“…T2-weighted images were registered to the Allen Brain Atlas 1 as described previously (Koch et al, 2017) using ANTX 2 , a custom MATLAB toolbox comprising a segmentation in SPMMouse 3 followed by non-linear warping of tissue probability maps in ELASTIX 4 . The calculated image transformation could then be applied to other images aligned with the T2-weighted scan, including TOF angiograms and lesion masks.…”

Section: Atlas Registrationmentioning

confidence: 99%

“…Lesion volume corrected for brain swelling was calculated as described previously (Koch et al, 2017). Briefly, ischemic tissue appearing hyperintense on T2-weighted images 24 h after stroke was manually delineated by an experienced researcher, carefully omitting ventricles, using ANALYZE 5.0 software (AnalyzeDirect, Overland Park, KS, United States), and masks of the same dimensionality as the T2-weighted image were exported in NIFTI format.…”

Section: Corrected Lesion Volumementioning

confidence: 99%

A Semiquantitative Non-invasive Measurement of PcomA Patency in C57BL/6 Mice Explains Variance in Ischemic Brain Damage in Filament MCAo

et al. 2020

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Numerous studies on experimental ischemic stroke use the filament middle cerebral artery occlusion (fMCAo) model in C57BL/6 mice, but lesion sizes in this strain are highly variable. A known contributor is variation in the posterior communicating artery (PcomA) patency. We therefore aimed to provide a semiquantitative non-invasive in vivo method to routinely assess PcomA patency. We included 43 male C57BL/6 mice from four independent studies using a transient 45 min fMCAo model. Edema-corrected lesion sizes were measured by magnetic resonance (MR) imaging 24 h after reperfusion. Timeof-flight MR angiography was performed 7 days before and 24 h after fMCAo. Scores of PcomA size measured 24 h after, but not scores measured 7 days before fMCAo were negatively correlated with lesion size. Variability in PcomA patency explained 30% of the variance in our cohort (p < 0.0001, coefficient of determination r 2 = 0.3). In a simulation using parameters typical for experimental stroke research, the power to detect a true effect of d = 1 between two groups increased by 15% when an according covariate was included in the statistical model. We have demonstrated that in vivo measurement of PcomA size is feasible and can lead to increased accuracy in assessing the effect of treatments.

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Atlas registration for edema-corrected MRI lesion volume in mouse stroke models

Cited by 53 publications

References 38 publications

Neuroprotection in Rats Following Ischaemia-Reperfusion Injury by GLP-1 Analogues—Liraglutide and Semaglutide

Neuroprotection in Rats Following Ischaemia-Reperfusion Injury by GLP-1 Analogues—Liraglutide and Semaglutide

Stage 1 Registered Report: Effect of deficient phagocytosis on neuronal survival and neurological outcome after temporary middle cerebral artery occlusion (tMCAo)

A Semiquantitative Non-invasive Measurement of PcomA Patency in C57BL/6 Mice Explains Variance in Ischemic Brain Damage in Filament MCAo

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