Alzheimer's disease may arise from an interaction between a conventional infective agent and a particular disease susceptibility (related to the HLA-A or B locus).
We determined the gene frequencies for the alleles of the HLA-linked complement markers C2, properdin factor B (BF), C4A (Rodgers) and C4B (Chido), and the red cell enzyme glyoxalase-I in 38 unrelated patients with senile dementia of the Alzheimer type, 42 patients with idiopathic Parkinson's disease, and 59 unaffected, aged-matched control blood donors.
This human prion gene has been mapped to human chromosome 20, negating a direct link between the prion protein and Down's syndrome or the amyloid of Alzheimer's disease.
There was no evidence of linkage of Alzheimer's disease with any of 27 phenotypic gene markers analyzed, but close linkage for the Rh and MNS blood group loci was excluded.
Instead, we observed a nonsignificant decrease in the Hp-1 gene frequency in the DAT population (0.34) as compared to our normal elderly comparison group (0.41).
Instead, we observed a nonsignificant decrease in the Hp-1 gene frequency in the DAT population (0.34) as compared to our normal elderly comparison group (0.41).
There was no evidence of linkage of Alzheimer's disease with any of 27 phenotypic gene markers analyzed, but close linkage for the Rh and MNS blood group loci was excluded.
There was no evidence of linkage of Alzheimer's disease with any of 27 phenotypic gene markers analyzed, but close linkage for the Rh and MNS blood group loci was excluded.
Instead, we observed a nonsignificant decrease in the Hp-1 gene frequency in the DAT population (0.34) as compared to our normal elderly comparison group (0.41).
There was no evidence of linkage of Alzheimer's disease with any of 27 phenotypic gene markers analyzed, but close linkage for the Rh and MNS blood group loci was excluded.