Christian Tackenberg, Dr.

Affiliations: 
Institute for Regenerative Medicine University of Zurich (UZH) 
Area:
Brain diseases, Alzheimers, stroke, stem cells
Website:
https://www.irem.uzh.ch/en/research/Group-R.-M.-Nitsch/Tackenberg.html
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"Christian Tackenberg"
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Publications

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Weber RZ, Grönnert L, Mulders G, et al. (2020) Characterization of the Blood Brain Barrier Disruption in the Photothrombotic Stroke Model. Frontiers in Physiology. 11: 586226
Tackenberg C, Kulic L, Nitsch RM. (2020) Familial Alzheimer's disease mutations at position 22 of the amyloid β-peptide sequence differentially affect synaptic loss, tau phosphorylation and neuronal cell death in an ex vivo system. Plos One. 15: e0239584
Rust R, Kirabali T, Grönnert L, et al. (2020) A Practical Guide to the Automated Analysis of Vascular Growth, Maturation and Injury in the Brain. Frontiers in Neuroscience. 14: 244
Tackenberg C, Nitsch RM. (2019) The secreted APP ectodomain sAPPα, but not sAPPβ, protects neurons against Aβ oligomer-induced dendritic spine loss and increased tau phosphorylation. Molecular Brain. 12: 27
Birnbaum JH, Wanner D, Gietl AF, et al. (2018) Oxidative stress and altered mitochondrial protein expression in the absence of amyloid-β and tau pathology in iPSC-derived neurons from sporadic Alzheimer's disease patients. Stem Cell Research. 27: 121-130
Penazzi L, Tackenberg C, Ghori A, et al. (2016) Aβ-mediated spine changes in the hippocampus are microtubule-dependent and can be reversed by a subnanomolar concentration of the microtubule-stabilizing agent epothilone D. Neuropharmacology. 105: 84-95
Derungs R, Camici GG, Spescha RD, et al. (2016) Genetic ablation of the p66Shc adaptor protein reverses cognitive deficits and improves mitochondrial function in an APP transgenic mouse model of Alzheimer’s disease Molecular Psychiatry
Penazzi L, Tackenberg C, Ghori A, et al. (2016) Aβ-mediated spine changes in the hippocampus are microtubule-dependent and can be reversed by a subnanomolar concentration of the microtubule-stabilizing agent epothilone D Neuropharmacology. 105: 84-95
Birnbaum JH, Bali J, Rajendran L, et al. (2015) Calcium flux-independent NMDA receptor activity is required for Aβ oligomer-induced synaptic loss. Cell Death & Disease. 6: e1791
Tackenberg C, Grinschgl S, Trutzel A, et al. (2013) NMDA receptor subunit composition determines beta-amyloid-induced neurodegeneration and synaptic loss. Cell Death & Disease. 4: e608
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