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Familial cases tend to have an earlier age at onset. Genetic defects in familial cases have been identified on chromosomes 21, 19, 14, 12 and 1. The so-called "early onset" cases of AD in persons in their 30's, 40's, and 50's may have a genetic basis. Less than 1% of early onset AD cases are linked to a genetic defect on chromosome 21 About half of early onset AD cases are linked to mutations in the presenilin 1 gene on chromosome 14. A presenilin 2 gene has been discovered on chromosome 1, but this defect accounts for less than 1% of cases. The more typical "late onset" cases of AD occurring after age 60 may have underlying genetic defects. A genetic locus on chromosome 19 encodes for a cholesterol transporter called apolipoprotein E (apoE). A genetic locus on chromosome 12 that encodes for alpha-2-macroglobulin may be found in 30% of AD cases. Mutations in the tau gene which codes for tau, a protein that is associated with microtubules, can be found in some AD cases.
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