Abstract：
:Modeling late-onset disorders such as Parkinson's disease (PD) using iPSC technology remains a challenge, as current differentiation protocols yield cells with the properties of fetal-stage cells. Here, we tested whether it is possible to accelerate aging in vitro to trigger late-onset disease phenotypes in an iPSC model of PD. In order to manipulate a factor that is involved in natural aging as well as in premature aging syndromes, we used telomere shortening as an age-inducing tool. We show that shortened telomeres result in age-associated as well as potentially disease-associated phenotypes in human pluripotent stem cell (hPSC)-derived midbrain dopamine (mDA) neurons. Our approach provides proof of concept for the further validation of telomere shortening as an induced-aging tool for late-onset-disease modeling.
journal_name
Cell Repjournal_title
Cell reportsauthors
Vera E,Bosco N,Studer Ldoi
10.1016/j.celrep.2016.09.062subject
Has Abstractpub_date
2016-10-18 00:00:00pages
1184-1192issue
4issn
2211-1247pii
S2211-1247(16)31318-3journal_volume
17pub_type
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