Haptoglobin types in Alzheimer's disease and senile dementia.

Abstract

There is much neuropathological evidence that Alzheimer's Disease and senile dementia are essentially identical disorders (Stam, 1962; McMenemey, 1963; Jamada and Mehraein, 1968; Lauter, 1970; Torvik, 1970). Family and genetic studies also give support to this opinion, for there appears to be a tendency for both senile dementia and Alzheimer's Disease towards familial aggregation (Zerbin-Rüdin, 1967; Pratt, 1970). An extensive Swedish study has given evidence that senile dementia is determined by a single autosomal dominent gene (Sjögrenet al., 1952). The difference in concordance rates between identical and non-identical twins with senile dementia is in agreement with this hypothesis (Kallmann, 1956). Furthermore, a number of families in which Alzheimer's Disease is transmitted as a regularly dominant trait have been described (Pratt, 1970). For the sporadic cases of Alzheimer's disease a cumulative polygenic action has been assumed (Larssonet al., 1963). Chromosome analysis of patients with Alzheimer's Disease and senile dementia has revealed certain abnormalities (Nielsen, 1968; Bergener and Jungklaass, 1970). Wheelan (1959) found that the MNSs blood groups appear to segregate with Alzheimer's Disease: however, another investigation failed to confirm a significant linkage between blood group genes and Alzheimer's Disease (Feldman, 1969).