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. 2012 Jul 15;2012:941232. doi: 10.1155/2012/941232

Figure 1.

Figure 1

Yeast models of (a) AD, based on amyloid-β42 expression; (b) PD, based on α-synuclein expression; (c) HD, based on Huntingtin's polyQ tract expression. (a) The toxic Aβ42 peptide expressed in yeast causes aggregation and moderate stress, but when expression is directed to the secretory pathway, the toxicity is increased. (b) At low expression levels, α-synuclein associates with the plasma membrane with no effect on cell viability. At doubling expression levels, α-synuclein redistributes from the cell surface into aggregates and induces toxicity. (c) Expression of a Huntingtin polyQ tract with 25 glutamines (normal length) does not lead to aggregation or toxicity. Expression of a polyQ tract with 103 glutamines (HD-associated expansion) leads to the formation of aggregates and toxicity (dependent on the presence of active prions).