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The ATPase Inhibitory Factor 1 (IF1) regulates the expression of the mitochondrial Ca2+ uniporter (MCU) via the AMPK/CREB pathway (2020)
Journal Article
Faccenda, D., Gorini, G., Jones, A., Thornton, C., Baracca, A., Solaini, G., & Campanella, M. (2020). The ATPase Inhibitory Factor 1 (IF1) regulates the expression of the mitochondrial Ca2+ uniporter (MCU) via the AMPK/CREB pathway. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, 118860

•IF1 regulates MCU-dependent mitochondrial Ca2+ uptake.

•IF1 loss induces MCU upregulation through activation of the AMPK/CREB pathway.

•OMA1 depletion restores physiological MCU levels and mitochondrial Ca2+ entry.

Zeta Inhibitory Peptide attenuates learning and memory by inducing NO-mediated downregulation of AMPA receptors (2020)
Journal Article
Bingor, A., Haham, T., Thornton, C., Stern-Bach, Y., & Yaka, R. (2020). Zeta Inhibitory Peptide attenuates learning and memory by inducing NO-mediated downregulation of AMPA receptors. Nature Communications, 11(1), https://doi.org/10.1038/s41467-020-17484-y

Zeta inhibitory peptide (ZIP), a PKMζ inhibitor, is widely used to interfere with the main- tenance of acquired memories. ZIP is able to erase memory even in the absence of PKMζ, via an unknown mechanism. We found that ZIP induces redistribution of t... Read More about Zeta Inhibitory Peptide attenuates learning and memory by inducing NO-mediated downregulation of AMPA receptors.

Neuroprotective Effects of Diabetes Drugs for the Treatment of Neonatal Hypoxia-Ischemia Encephalopathy (2020)
Journal Article
Poupon-Bejuit, L., Rocha-Ferreira, E., Thornton, C., Hagberg, H., & Rahim, A. A. (2020). Neuroprotective Effects of Diabetes Drugs for the Treatment of Neonatal Hypoxia-Ischemia Encephalopathy. Frontiers in Cellular Neuroscience, 14, https://doi.org/10.3389/fncel.2020.00112

The perinatal period represents a time of great vulnerability for the developing brain. A variety of injuries can result in death or devastating injury causing profound neurocognitive deficits. Hypoxic-ischemic neonatal encephalopathy (HIE) remains t... Read More about Neuroprotective Effects of Diabetes Drugs for the Treatment of Neonatal Hypoxia-Ischemia Encephalopathy.

Interneuron Development Is Disrupted in Preterm Brains With Diffuse White Matter Injury: Observations in Mouse and Human (2019)
Journal Article
Stolp, H. B., Fleiss, B., Arai, Y., Supramaniam, V., Vontell, R., Birtles, S., Yates, A., Baburamani, A. A., Thornton, C., Rutherford, M., Edwards, A. D., & Gressens, P. (2019). Interneuron Development Is Disrupted in Preterm Brains With Diffuse White Matter Injury: Observations in Mouse and Human. Frontiers in Physiology, 10(955), https://doi.org/10.3389/fphys.2019.00955

Preterm brain injury, occurring in approximately 30% of infants born

Post-mortem Characterisation of a Case With an ACTG1 Variant, Agenesis of the Corpus Callosum and Neuronal Heterotopia (2019)
Journal Article
Vontell, R., Supramaniam, V. G., Davidson, A., Thornton, C., Marnerides, A., Holder-Espinasse, M., Lillis, S., Yau, S., Jansson, M., Hagberg, H. E., & Rutherford, M. A. (2019). Post-mortem Characterisation of a Case With an ACTG1 Variant, Agenesis of the Corpus Callosum and Neuronal Heterotopia. Frontiers in Physiology, 10, https://doi.org/10.3389/fphys.2019.00623

Cytoplasmic Actin Gamma 1 (ACTG1) gene variant are autosomal dominant and can cause CNS anomalies (Baraitser Winter Malformation Syndrome; BWMS). ACTG1 anomalies in offspring include agenesis of the corpus callosum (ACC) and neuronal heterotopia whic... Read More about Post-mortem Characterisation of a Case With an ACTG1 Variant, Agenesis of the Corpus Callosum and Neuronal Heterotopia.

Magnesium induces preconditioning of the neonatal brain via profound mitochondrial protection (2019)
Journal Article
Koring, G., Leverin, A. L., Nair, S., Schwendimann, L., Ek, J., Carlsson, Y., Gressens, P., Thornton, C., Wang, X., Mallard, C., & Hagberg, H. (2019). Magnesium induces preconditioning of the neonatal brain via profound mitochondrial protection. https://doi.org/10.1177/0271678X17746132

Magnesium sulphate (MgSO4) given to women in preterm labor reduces cerebral palsy in their offspring but the mechanism behind this protection is unclear, limiting its effective, safe clinical implementation. Previous studies suggest that MgSO4 is not... Read More about Magnesium induces preconditioning of the neonatal brain via profound mitochondrial protection.

Neuroprotective exendin-4 enhances hypothermia therapy in a model of hypoxic-ischaemic encephalopathy (2018)
Journal Article
Rocha-Ferreira, E., Poupon, L., Zelco, A., Leverin, A. L., Nair, S., Jonsdotter, A., Carlsson, Y., Thornton, C., Hagberg, H., & Rahim, A. A. (2018). Neuroprotective exendin-4 enhances hypothermia therapy in a model of hypoxic-ischaemic encephalopathy. Brain, 141(10), 2925-2942. https://doi.org/10.1093/brain/awy220

Hypoxic-ischaemic encephalopathy remains a global health burden. Despite medical advances and treatment with therapeutic hypothermia, over 50% of cooled infants are not protected and still develop lifelong neurodisabilities, including cerebral palsy.... Read More about Neuroprotective exendin-4 enhances hypothermia therapy in a model of hypoxic-ischaemic encephalopathy.

TWEAK Receptor Deficiency Has Opposite Effects on Female and Male Mice Subjected to Neonatal Hypoxia-Ischemia (2018)
Journal Article
Kichev, A., Baburamani, A. A., Vontell, R., Gressens, P., Burkly, L., Thornton, C., & Hagberg, H. (2018). TWEAK Receptor Deficiency Has Opposite Effects on Female and Male Mice Subjected to Neonatal Hypoxia-Ischemia. Frontiers in Neurology, 9(230), https://doi.org/10.3389/fneur.2018.00230

Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) is a multifunctional cytokine member of the TNF family. TWEAK binds to its only known receptor, Fn14, enabling it to activate downstream signaling processes in response to tissue inju... Read More about TWEAK Receptor Deficiency Has Opposite Effects on Female and Male Mice Subjected to Neonatal Hypoxia-Ischemia.

Voxel-wise comparisons of cellular microstructure and diffusion-MRI in mouse hippocampus using 3D Bridging of Optically-clear histology with Neuroimaging Data (3D-BOND) (2018)
Journal Article
Stolp, H. B., Ball, G., So, P.-W., Tournier, J.-D., Jones, M., Thornton, C., & Edwards, A. D. (2018). Voxel-wise comparisons of cellular microstructure and diffusion-MRI in mouse hippocampus using 3D Bridging of Optically-clear histology with Neuroimaging Data (3D-BOND). https://doi.org/10.1038/s41598-018-22295-9

A key challenge in medical imaging is determining a precise correspondence between image properties and tissue microstructure. This comparison is hindered by disparate scales and resolutions between medical imaging and histology. We present a new tec... Read More about Voxel-wise comparisons of cellular microstructure and diffusion-MRI in mouse hippocampus using 3D Bridging of Optically-clear histology with Neuroimaging Data (3D-BOND).

Lipopolysaccharide-induced alteration of mitochondrial morphology induces a metabolic shift in microglia modulating the inflammatory response in vitro and in vivo (2018)
Journal Article
Nair, S., Sobotka, K. S., Joshi, P., Gressens, P., Fleiss, B., Thornton, C., Mallard, C., & Hagberg, H. (2018). Lipopolysaccharide-induced alteration of mitochondrial morphology induces a metabolic shift in microglia modulating the inflammatory response in vitro and in vivo. Glia, https://doi.org/10.1002/glia.23587

Accumulating evidence suggests that changes in the metabolic signature of microglia underlie their response to inflammation. We sought to increase our knowledge of how pro‐inflammatory stimuli induce metabolic changes. Primary microglia exposed to li... Read More about Lipopolysaccharide-induced alteration of mitochondrial morphology induces a metabolic shift in microglia modulating the inflammatory response in vitro and in vivo.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) signaling and cell death in the immature central nervous system after hypoxia-ischemia and inflammation (2014)
Journal Article
Kichev, A., Rousset, C. I., Baburamani, A. A., Levison, S. W., Wood, T. L., Gressens, P., Thornton, C., & Hagberg, H. (2014). Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) signaling and cell death in the immature central nervous system after hypoxia-ischemia and inflammation. Journal of Biological Chemistry, 289(13), 9430-9439. https://doi.org/10.1074/jbc.M113.512350

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family. The interaction of TRAIL with death receptor 4 (DR4) and DR5 can trigger apoptotic cell death. The aim of this study was to investigate the role of TRAIL s... Read More about Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) signaling and cell death in the immature central nervous system after hypoxia-ischemia and inflammation.