Aim: We aimed to investigate the neuroprotective role of adalimumab based onthe hypothesis that "TNF-alpha inhibitor adalimumab may affect inflammationrelated neuronal injury due to its anti-inflammatory effect".Methods: To investigate the effects of adalimumab, we induced brain injury inmice using a cold trauma model and evaluated the underlying cell survival/ deathmechanisms via cresyl violet and calculated infarct/edema volume with imageanalyze system.Results: Although our data indicated a tendency to decreased infarct and edemavolume, these findings are not significant statistically.Conclusion: To the best of our knowledge, this is the first study evaluating theneuroprotective effect of adalimumab on injured neurons.
📌 3 Key Takeaways
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Objective & Hypothesis:Aim: We aimed to investigate the neuroprotective role of adalimumab based onthe hypothesis that "TNF-alpha inhibitor adalimumab may affect inflammationrelated neuronal injury due to its anti-inflammatory effect".Methods: To investigate the effects of adalimumab, we induced brain injury inmice using a cold trauma model and evaluated the underlying cell survival/ deathmechanisms via cresyl violet and calculated infarct/edema volume with imageanalyze system.Results: Although our data indicated a tendency to decreased infarct and edemavolume, these findings are not significant statistically.Conclusion: To the best of our knowledge, this is the first study evaluating theneuroprotective effect of adalimumab on injured neurons.
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Key Findings & Data:Aim: We aimed to investigate the neuroprotective role of adalimumab based onthe hypothesis that "TNF-alpha inhibitor adalimumab may affect inflammationrelated neuronal injury due to its anti-inflammatory effect".Methods: To investigate the effects of adalimumab, we induced brain injury inmice using a cold trauma model and evaluated the underlying cell survival/ deathmechanisms via cresyl violet and calculated infarct/edema volume with imageanalyze system.Results: Although our data indicated a tendency to decreased infarct and edemavolume, these findings are not significant statistically.Conclusion: To the best of our knowledge, this is the first study evaluating theneuroprotective effect of adalimumab on injured neurons.
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Conclusion & Impact:Aim: We aimed to investigate the neuroprotective role of adalimumab based onthe hypothesis that "TNF-alpha inhibitor adalimumab may affect inflammationrelated neuronal injury due to its anti-inflammatory effect".Methods: To investigate the effects of adalimumab, we induced brain injury inmice using a cold trauma model and evaluated the underlying cell survival/ deathmechanisms via cresyl violet and calculated infarct/edema volume with imageanalyze system.Results: Although our data indicated a tendency to decreased infarct and edemavolume, these findings are not significant statistically.Conclusion: To the best of our knowledge, this is the first study evaluating theneuroprotective effect of adalimumab on injured neurons.
🔬Design:Modeling & Simulation
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters
Abstract
Aim: We aimed to investigate the neuroprotective role of adalimumab based onthe hypothesis that "TNF-alpha inhibitor adalimumab may affect inflammationrelated neuronal injury due to its anti-inflammatory effect".Methods: To investigate the effects of adalimumab, we induced brain injury inmice using a cold trauma model and evaluated the underlying cell survival/ deathmechanisms via cresyl violet and calculated infarct/edema volume with imageanalyze system.Results: Although our data indicated a tendency to decreased infarct and edemavolume, these findings are not significant statistically.Conclusion: To the best of our knowledge, this is the first study evaluating theneuroprotective effect of adalimumab on injured neurons.
Özet
Amaç: “TNF-alfa inhibitörü Adalimumab’ın, anti-inflamatuvar etkisi nedeniyle inflamasyonla ilişkili nöronal hasarı etkileyebileceği” hipotezine dayanarak adalimumab’ın nöroprotektif rolünü araştırmayı amaçladık. Metotlar: Adalimumab’ın etkilerini araştırmak için soğuk travma modelini kullanarak farelerde beyin hasarı oluşturduk ve krezil viyole boyasıyla hücre sağ-kalım/ölüm oranları ile görüntü analiz sistemi ile hesaplanan infarktüs/ödem hacmini değerlendirdik. Bulgular: Verilerimiz infarkt ve ödem hacminde azalma eğilimi göstermesine rağmen istatistiksel olarak anlamlı değildir. Sonuç: Bildiğimiz kadarıyla çalışmamız adalimumab’ın hasarlı nöronlar üzerindeki nöroprotektif etkisini değerlendiren ilk çalışmadır.
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Cite This Article
GÜNAL, M. Y., TÖNÜK, Ş. B., ŞAKUL, A. A. S., ÖZDEMİR, E. M., ÇANKAYA, S. (2022). Investigation of The Effect of Adalimumab on Experimental Brain Injury in Mice. Acta Medica Alanya, Cilt: 3 - Sayı: 3, 306–310. https://ajindex.com/articles/425858
Narayan RK, Michel ME, Ansell B, Baethmann A, Biegon A, Bracken MB, et al. Clinical trials in head injury. Journal of neurotrauma. 2002;19(5):503-57. doi: 10.1089/089771502753754037
Maas AI, Roozenbeek B, Manley GT. Clinical trials in traumatic brain injury: past experience and current developments. Neurotherapeutics. 2010;7(1):115-26. doi: 10.1016/j.nurt.2009.10.022
Werner C, Engelhard K. Pathophysiology of traumatic brain injury. Br J Anaesth. 2007;99(1):4-9. doi: 10.1093/bja/aem131
Burmester GR, Mease P, Dijkmans BA, Gordon K, Lovell D, Panaccione R, et al. Adalimumab safety and mortality rates from global clinical trials of six immune-mediated inflammatory diseases. Ann Rheum Dis. 2009;68(12):1863-9. doi: 10.1136/ ard.2008.102103
Clark J, Vagenas P, Panesar M, Cope AP. What does tumour necrosis factor excess do to the immune system long term? Annals of the Rheumatic Diseases. 2005;64:70-6. doi: 10.1136/ard.2005.042523
Woodcock T, Morganti-Kossmann MC. The role of markers of inflammation in traumatic brain injury. Front Neurol. 2013;4:18. doi: 10.3389/fneur.2013.00018
Mitoma H, Horiuchi T, Tsukamoto H, Ueda N. Molecular mechanisms of action of anti-TNF-alpha agents - Comparison among therapeutic TNF-alpha antagonists. Cytokine. 2018;101:56-63. doi: 10.1016/j.cyto.2016.08.014
Shohet JM, Bergamaschini L, Davis AE, Carroll MC. Localization of the human complement component C3 binding site on the IgG heavy chain. J Biol Chem. 1991;266(28):18520-4. PMID: 1917974 9. Tracey D, Klareskog L, Sasso EH, Salfeld JG, Tak PP. Tumor necrosis factor antagonist mechanisms of action: a comprehensive review. Pharmacol Ther. 2008;117(2):244-79. doi: 10.1016/j.pharmthera.2007.10.001 10. Yu F, Gudmundsdotter L, Akal A, Gunneriusson E, Frejd F, Nygren PA. An affibody-adalimumab hybrid blocks combined IL-6 and TNF-triggered serum amyloid A secretion in vivo. MAbs. 2014;6(6):1598-607. doi: 10.4161/mabs.36089
Yan HY, Semple KM, Gonzalez CM, Howard KE. Bone marrow-liver-thymus (BLT) immune humanized mice as a model to predict cytokine release syndrome. Transl Res. 2019;210:43-56. doi: 10.1016/j.trsl.2019.04.007
Park J, Lee SY, Shon J, Kim K, Lee HJ, Kim KA, et al. Adalimumab improves cognitive impairment, exerts neuroprotective effects and attenuates neuroinflammation in an A beta(1-40)-injected mouse model of Alzheimer's disease. Cytotherapy. 2019;21(6):671-82. doi: 10.1016/j.jcyt.2019.04.054