The three types of<unk>  are autosomal recessive. Both parents must be carriers for a child to be affected. If both parents are carriers, the chance of the<unk>  is one in four, or 25%, with each pregnancy for an affected child. Genetic counseling and genetic testing are recommended for families who may be carriers of mutations. Each type has been linked to particular mutations. In all, about 80 known GBA gene mutations are grouped into three main types: * Type I (N370S homozygote), the most common, also called the "non-neuropathic" type occurs mainly in Ashkenazi Jews, at 100 times the occurrence in the general populace. The median age at diagnosis is 28 years of age, and life expectancy is mildly decreased. * Type II (one or two alleles L444P) is characterized by neurological problems in small children. The enzyme is hardly released into the lysosomes. Prognosis is poor: most die before the age of three. * Type III (also one or two copies of L444P, possibly delayed by protective polymorphisms) occurs in Swedish patients from the Norrbotten region. This group develops the<unk>  somewhat later, but most die before their 30th birthday. The<unk> -causing mutations may have entered the Ashkenazi Jewish gene pool in the early Middle Ages (48–55 generations ago).
Gaucher's disease
Glycogen storage disease type III
Glycogen storage disease type 0
Glycogen storage disease type IX
Glycogen storage disease type IV
Glycogen storage disease type I
Glycogen storage disease type II
Glycogen storage disease type VI