For example, de novo mutations (C to G in
fibroblast growth factor receptor 2 (FGFR2) gene) in 57 Apert cases were all of paternal
origin; and the age of the fathers was significantly increased at the time of birth with a mean
of 33.0 years of age compared with 30.7 year of age in an age-matched control group [3]. A
man's risk to father a child with Apert syndrome when more than 50-years-old is 9.5-fold
higher than that of a man 25-to 29-years-old [4]. In addition to several diseases with clear
Mendelian inheritance, advanced paternal age is also linked to an increased risk for diseases
with a genetic component such as childhood cancers [5–7], diabetes mellitus type I [8],
multiple sclerosis [9], autism [10] and congenital malformations [11] and others. The
association between paternal age and increased risk for diseases in offspring may be at least
partially ascribed to mutagenesis in male gametes [12–16].