CPL - Chalmers Publication Library
| Utbildning | Forskning | Styrkeområden | Om Chalmers | In English In English Ej inloggad.

Amyloid-beta peptide-induced cytotoxicity and mitochondrial dysfunction in yeast

Xin Chen (Institutionen för biologi och bioteknik, Systembiologi) ; Dina Petranovic (Institutionen för biologi och bioteknik, Systembiologi)
Fems Yeast Research (1567-1356). Vol. 15 (2015), 6, p. Art. no. fov061.
[Artikel, refereegranskad vetenskaplig]

Alzheimer's disease (AD) is the most common neurodegenerative disease, characterized by deposits of amyloid-beta(A beta) peptides. However, the underlying molecular mechanisms of neuron cell dysfunction and cell death in AD still remain poorly understood. Yeast Saccharomyces cerevisiae shares many conserved biological processes with all eukaryotic cells, including human neurons. Thanks to relatively simple and quick genetic and environmental manipulations, the large knowledge base and data collections, this organism has become a valuable tool to unravel fundamental intracellular mechanisms underlying neurodegeneration. In this study, we have used yeast as a model system to study the effects of intracellular A beta peptides and we found that cells constitutively producing native A beta directed to the secretory pathway exhibited a lower growth rate, lower biomass yield, lower respiratory rate, increased oxidative stress, hallmarks of mitochondrial dysfunction and ubiquitin-proteasome system dysfunction. These findings are relevant for better understanding the role of A beta in cell stress and cell damage.

Nyckelord: Amyloid-beta, Alzheimer's disease, yeast, mitochondria, oxidative stress, ubiquitin-proteasome system



Denna post skapades 2015-10-21. Senast ändrad 2016-07-15.
CPL Pubid: 224563

 

Läs direkt!


Länk till annan sajt (kan kräva inloggning)


Institutioner (Chalmers)

Institutionen för biologi och bioteknik, Systembiologi

Ämnesområden

Neurologi

Chalmers infrastruktur