Apolipoprotein E genotype and amyloid load in Alzheimer disease and control brains

We investigated the effect of apolipoprotein E (apoE) genotype on amyloid load in the frontal and cerebellar cortices of 24 patients with definite Alzheimer disease (AD) and 19 controls. Amyloid load was examined by using two methods: 1) acid-extractable amyloid beta-protein (Aβ) and insoluble Aβ levels of frontal and cerebellar cortices were measured by using enzyme-linked immunosorbent assay, and 2) all types of amyloid plaques and neurofibrillary tangles (NFT) in the frontal cortices were counted after silver staining. Acid-extractable Aβ and insoluble Aβ levels were higher in AD brains than controls, although there was an overlap between the groups. Acid-extractable Aβ and insoluble Aβ levels were higher from AD and controls with the apoE ε4 alleles than those without such alleles. However, the differences did not reach statistical significance in AD group. There was no correlation between acid-extractable Aβ or insoluble Aβ levels and the number of amyloid plaques in AD and control brains. However, insoluble Aβ levels correlated positively with the number of NFT in AD brains. Our results show that although apoE ε4 influences the accumulation of Aβ, multiple processes may be involved in deposition of Aβ in the brain.