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Scripps Research scientists create new genetic model of premature aging diseases
Date:4/29/2011

search, scientists set out to block the protein production of the LMNA gene in zebrafish. This resulted in apoptosis or programmed cell death, as well as interruption of the normal cell cycle. Deletion of some specific amino acid residues in the lamin A protein also produced aging in embryonic zebrafish.

Intriguingly, the study also found that farnestyl transferase inhibitor (FTI), a new class of anti-cancer drugs, reduced abnormalities in the nuclear membrane and prevented significant aging in the embryonic zebrafish models, which survived to adulthood but with a shortened lifespan.

"Utilizing our 'embryonic senescence' zebrafish model, our next goal will be to find modifier genes as well as chemical compounds to reverse accelerated aging and restore the normal aging process," Kishi said. "These findings could contribute to healthy aging in normal individuals, because the moderate defects of lamin A are also associated with the normal aging process."


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Contact: Mika Ono
mikaono@scripps.edu
858-784-2052
Scripps Research Institute
Source:Eurekalert

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