A hypothesis that aging results from defects in genetically produced proteins.
The hypothesis is presented that our life span is genetically programmed and that it is possible that a defect in produced proteins encoded by the 'longevity' gene is a cause of aging. A study of correlations between defective enzyme activity in two diseases characterized by premature aging (progeria and Werner's syndrome) could assist in elucidating the common mechanism for all aging processes.
Secerbegovic
S
S
Department of Biology, University of Sarajevo, Bosnia.
D000328:Adult; D000368:Aged; D000375:Aging / Q000235:genetics* / Q000378:metabolism; D002648:Child; D004265:DNA Helicases / Q000235:genetics; D006801:Humans; D008136:Longevity / Q000235:genetics; D008954:Models, Biological; D011371:Progeria / Q000201:enzymology / Q000235:genetics; D011506:Proteins / Q000235:genetics*; D019098:Telomerase / Q000235:genetics; D016615:Telomere / Q000235:genetics / Q000648:ultrastructure; D014898:Werner Syndrome / Q000201:enzymology / Q000235:genetics
D011506:Proteins; D019098:Telomerase; D004265:DNA Helicases