Hutchinson-Gilford progeria syndrome (HGPS, progeria) is an extremely rare 
premature aging disorder affecting children, with a disease incidence of ∼1 in 
18 million individuals. HGPS is usually caused by a de novo point mutation in 
exon 11 of the LMNA gene (c.1824C>T, p.G608G), resulting in the increased usage 
of a cryptic splice site and production of a truncated unprocessed lamin A 
protein named progerin. Since the genetic cause for HGPS was published in 2003, 
numerous potential treatment options have rapidly emerged. Strategies to 
interfere with the post-translational processing of lamin A, to enhance progerin 
clearance, or directly target the HGPS mutation to reduce the progerin-producing 
alternative splicing of the LMNA gene have been developed. Here, we give an 
up-to-date resume of the contributions made by our and other research groups to 
the growing list of different candidate treatment strategies that have been 
tested, both in vitro, in vivo in mouse models for HGPS and in clinical trials 
in HGPS patients.