This Article  • Full text  • PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citing articles on ISI (2)  • Contact me when this article is cited  Related Content  • Similar articles in JAMA  Topic Collections  • Genetic Counseling/ Testing/ Therapy  • Alert me on articles by topic

Bridget M. Kuehn

JAMA. 2006;295:876-878.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Scientists are racing toward a better understanding of the cellular and molecular basis of Hutchinson-Gilford progeria syndrome, a rare disease that speeds the aging process so much that children with the disorder die from diseases typically associated with advanced age, usually in their early teens.

Since the 2003 discovery that a mutation in the LMNA gene causes progeria, scientists have developed several mouse models for the disorder, amassed a growing body of evidence regarding the disease's molecular and cellular basis, and devised experimental treatment strategies. Whether such treatments would be safe and effective for children with progeria remains to be determined, but scientists and advocates are buoyed by the swift pace of progress.

Scientists are studying potential treatments for progeria, a disorder that causes children, such as this 5-year-old girl, to develop symptoms associated with advanced age. (Photo credit: John Hurley/Progeria Research Foundation)

"We have been incredibly . . . [Full Text of this Article]

FORM AND FUNCTION