Background: alpha2-Macroglobulin (A2M) forms the complex with amyloid beta-protein (Abeta) and is associated with degradation of Abeta. It has been reported that the A2M gene (A2M) exon 18 splice acceptor deletion polymorphism influences the development of AD, regardless of apolipoprotein E-epsilon4 (APOE-epsilon4) status.
Objective: To determine the effect of A2M polymorphism on the development of AD and AD-type neuropathologic changes.
Methods: The authors examined the A2M and APOE genotypes, the densities of the senile plaques (SPs), SPs with dystrophic neurites (NPs), and neurofibrillary tangles (NFTs) in the brains of 62 postmortem-confirmed sporadic AD and 90 nondemented patients from an autopsy series of elderly Japanese subjects.
Results: There was no association of the A2M polymorphism with AD, age at onset, or duration of illness in AD. The A2M polymorphism was not associated with the SPs, NPs, or NFTs in AD or nondemented patients. The results remained insignificant, even when the A2M genotype groups were divided into subgroups by APOE-epsilon4 status.
Conclusion: The A2M polymorphism does not affect the development of sporadic AD or formation of AD-type neuropathologic changes.