![Ioannis DAFNIS | PhD | National Center for Scientific Research Demokritos, Athens | ncsr | Institute of Biosciences and Applications (IB-A) Ioannis DAFNIS | PhD | National Center for Scientific Research Demokritos, Athens | ncsr | Institute of Biosciences and Applications (IB-A)](https://i1.rgstatic.net/ii/profile.image/1001634352070661-1615819647156_Q128/Amalia-Megarioti.jpg)
Ioannis DAFNIS | PhD | National Center for Scientific Research Demokritos, Athens | ncsr | Institute of Biosciences and Applications (IB-A)
![Ioannis DAFNIS | PhD | National Center for Scientific Research Demokritos, Athens | ncsr | Institute of Biosciences and Applications (IB-A) Ioannis DAFNIS | PhD | National Center for Scientific Research Demokritos, Athens | ncsr | Institute of Biosciences and Applications (IB-A)](https://i1.rgstatic.net/ii/profile.image/1019806471946241-1620152218609_Q128/Eirini-Panagopoulou-3.jpg)
Ioannis DAFNIS | PhD | National Center for Scientific Research Demokritos, Athens | ncsr | Institute of Biosciences and Applications (IB-A)
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An apolipoprotein E4 fragment can promote intracellular accumulation of amyloid peptide beta 42 - Dafnis - 2010 - Journal of Neurochemistry - Wiley Online Library
![Activation of both transforming growth factor-β and bone morphogenetic protein signalling pathways upon traumatic brain injury restrains pro-inflammatory and boosts tissue reparatory responses of reactive astrocytes and microglia. - Abstract - Europe Activation of both transforming growth factor-β and bone morphogenetic protein signalling pathways upon traumatic brain injury restrains pro-inflammatory and boosts tissue reparatory responses of reactive astrocytes and microglia. - Abstract - Europe](https://europepmc.org/articles/PMC7425383/bin/fcz028f9.jpg)
Activation of both transforming growth factor-β and bone morphogenetic protein signalling pathways upon traumatic brain injury restrains pro-inflammatory and boosts tissue reparatory responses of reactive astrocytes and microglia. - Abstract - Europe
![apoE3[K146N/R147W] acts as a dominant negative apoE form that prevents remnant clearance and inhibits the biogenesis of HDL[S] - Journal of Lipid Research apoE3[K146N/R147W] acts as a dominant negative apoE form that prevents remnant clearance and inhibits the biogenesis of HDL[S] - Journal of Lipid Research](https://els-jbs-prod-cdn.jbs.elsevierhealth.com/cms/attachment/3aa3fbdd-4694-4a40-a519-58d09bf3e312/gr5_lrg.jpg)
apoE3[K146N/R147W] acts as a dominant negative apoE form that prevents remnant clearance and inhibits the biogenesis of HDL[S] - Journal of Lipid Research
![Ioannis DAFNIS | PhD | National Center for Scientific Research Demokritos, Athens | ncsr | Institute of Biosciences and Applications (IB-A) Ioannis DAFNIS | PhD | National Center for Scientific Research Demokritos, Athens | ncsr | Institute of Biosciences and Applications (IB-A)](https://www.researchgate.net/publication/260916960/figure/fig4/AS:931759948570625@1599160291339/Protease-digestion-sensitivity-of-WT-apoE4-and-apoE4L28P-WT-and-mutant-apoE4-were_Q320.jpg)
Ioannis DAFNIS | PhD | National Center for Scientific Research Demokritos, Athens | ncsr | Institute of Biosciences and Applications (IB-A)
![apoE3[K146N/R147W] acts as a dominant negative apoE form that prevents remnant clearance and inhibits the biogenesis of HDL. - Abstract - Europe PMC apoE3[K146N/R147W] acts as a dominant negative apoE form that prevents remnant clearance and inhibits the biogenesis of HDL. - Abstract - Europe PMC](https://europepmc.org/articles/PMC4076092/bin/1310fig1.jpg)
apoE3[K146N/R147W] acts as a dominant negative apoE form that prevents remnant clearance and inhibits the biogenesis of HDL. - Abstract - Europe PMC
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Mechanistic insight into the capacity of natural polar phenolic compounds to abolish Alzheimer's disease-associated pathogenic effects of apoE4 forms - ScienceDirect
![Molecular Basis for Increased Risk for Late-onset Alzheimer Disease Due to the Naturally Occurring L28P Mutation in Apolipoprotein E4* - Journal of Biological Chemistry Molecular Basis for Increased Risk for Late-onset Alzheimer Disease Due to the Naturally Occurring L28P Mutation in Apolipoprotein E4* - Journal of Biological Chemistry](https://els-jbs-prod-cdn.jbs.elsevierhealth.com/cms/attachment/deae7e0a-7e72-40a9-b611-f73ec33d1f07/gr5.jpg)
Molecular Basis for Increased Risk for Late-onset Alzheimer Disease Due to the Naturally Occurring L28P Mutation in Apolipoprotein E4* - Journal of Biological Chemistry
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apoE3[K146N/R147W] acts as a dominant negative apoE form that prevents remnant clearance and inhibits the biogenesis of HDL[S] - Journal of Lipid Research
![Ioannis DAFNIS | PhD | National Center for Scientific Research Demokritos, Athens | ncsr | Institute of Biosciences and Applications (IB-A) Ioannis DAFNIS | PhD | National Center for Scientific Research Demokritos, Athens | ncsr | Institute of Biosciences and Applications (IB-A)](https://i1.rgstatic.net/ii/profile.image/372887526625281-1465914722139_Q512/Ioannis-Dafnis.jpg)