Display options
Cite
Braun RJ, Sommer C, Leibiger C, et al. Modeling non-hereditary mechanisms of Alzheimer disease during apoptosis in yeast. Microb Cell. 2015;2(4):136-138doi: 10.15698/mic2015.04.199.
Braun, R. J., Sommer, C., Leibiger, C., Gentier, R. J., Dumit, V. I., Paduch, K., Eisenberg, T., Habernig, L., Trausinger, G., Magnes, C., Pieber, T., Sinner, F., Dengjel, J., Leeuwen, F. W., Kroemer, G., & Madeo, F. (2015). Modeling non-hereditary mechanisms of Alzheimer disease during apoptosis in yeast. Microbial cell (Graz, Austria), 2(4), 136-138. https://doi.org/10.15698/mic2015.04.199
Braun, Ralf J, et al. "Modeling non-hereditary mechanisms of Alzheimer disease during apoptosis in yeast." Microbial cell (Graz, Austria) vol. 2,4 (2015): 136-138. doi: https://doi.org/10.15698/mic2015.04.199
Braun RJ, Sommer C, Leibiger C, Gentier RJ, Dumit VI, Paduch K, Eisenberg T, Habernig L, Trausinger G, Magnes C, Pieber T, Sinner F, Dengjel J, Leeuwen FW, Kroemer G, Madeo F. Modeling non-hereditary mechanisms of Alzheimer disease during apoptosis in yeast. Microb Cell. 2015 Mar 20;2(4):136-138. doi: 10.15698/mic2015.04.199. PMID: 28357285; PMCID: PMC5348975.
Copy Download .nbib Format: NLM
Share it on

Microb Cell. 2015 Mar 20;2(4):136-138. doi: 10.15698/mic2015.04.199.

Modeling non-hereditary mechanisms of Alzheimer disease during apoptosis in yeast.

Microbial cell (Graz, Austria)

Ralf J Braun, Cornelia Sommer, Christine Leibiger, Romina J Gentier, Verónica I Dumit, Katrin Paduch, Tobias Eisenberg, Lukas Habernig, Gert Trausinger, Christoph Magnes, Thomas Pieber, Frank Sinner, Jörn Dengjel, Fred W V Leeuwen, Guido Kroemer, Frank Madeo

Affiliations

  1. Institute of Cell Biology, University of Bayreuth, 95440 Bayreuth, Germany.
  2. Institute of Molecular Biosciences, NAWI Graz, University of Graz, 8010 Graz, Austria. ; BioTechMed-Graz, 8010 Graz, Austria.
  3. Department of Neuroscience, Faculty of Health, Medicine and Life Sciences, Maastricht University, 6229 ER Maastricht, The Netherlands.
  4. FRIAS Freiburg Institute for Advanced Studies, Department of Dermatology, Medical Center, ZBSA Center for Biological Systems Analysis, BIOSS Centre for Biological Signalling Studies, University of Freiburg, 79104 Freiburg, Germany.
  5. Institute of Molecular Biosciences, NAWI Graz, University of Graz, 8010 Graz, Austria.
  6. HEALTH Institute for Biomedicine and Health Sciences, Joanneum Research, 8010 Graz, Austria.
  7. HEALTH Institute for Biomedicine and Health Sciences, Joanneum Research, 8010 Graz, Austria. ; Division of Endocrinology and Metabolism, Medical University of Graz, 8036 Graz, Austria.
  8. Apoptosis, Cancer & Immunity Laboratory, Team 11, Equipe labellisée Ligue contre le Cancer, INSERM Cordeliers Research Cancer, 75006 Paris, France. ; Institute of Cell Biology, University of Bayreuth, 95440 Bayreuth, Germany. ; Institute of Cell Biology, University of Bayreuth, 95440 Bayreuth, Germany. ; Institute of Cell Biology, University of Bayreuth, 95440 Bayreuth, Germany.

PMID: 28357285 PMCID: PMC5348975 DOI: 10.15698/mic2015.04.199

Abstract

Impaired protein degradation and mitochondrial dysfunction are believed to contribute to neurodegenerative disorders, including Alzheimer disease (AD). In patients suffering from non-hereditary AD, UBB

Keywords: aging; apoptosis; autophagy; cell death; microbes; microbial research; microbiome; neurodegeneration; unicellular organism

Conflict of interest statement

Conflict of interest: The authors declare no conflict of interest.

Publication Types