al. 2011). iPSC-derived dopaminergic neurons derived from these patients show molecular phenotypes characteristic of the disease, suggesting that such pathological events can be detected and monitored (Chung et al. 2013). An alternative strategy is to accelerate ageing or disease progression using stressors such as rotenone, MG-132 or concanamycin A (Cooper et al. 2012; Nguyen et al. 2011), or through expression of Progerin, a truncated form of lamin A that is associated with Hutchinson–Gilford progeria syndrome, a premature ageing disorder (Miller et al. 2013). Whilst Progerin expression has been shown to accelerate cellular markers of ageing such as DNA damage and heterochromatic chromatin modifications (Miller et al. 2013), it is still unclear to what extent such treatments fully recapitulate the effects of old age.
