Pirttilä T, Soininen H, Mehta P D, Heinonen O, Lehtimäki T, Bogdanovic N, Paljärvi L, Kim K S, Kosunen O, Winblad B, Riekkinen P, Wisniewski H M
Institute for Basic Research in Developmental Disabilities, Staten Island, NY 10314, USA.
Neurobiol Aging. 1997 Jan-Feb;18(1):121-7. doi: 10.1016/s0197-4580(96)00204-7.
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 (A beta) and insoluble A beta 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 A beta and insoluble A beta levels were higher in AD brains than controls, although there was an overlap between the groups. Acid-extractable A beta and insoluble A beta levels were higher from AD and controls with the apoE epsilon 4 alleles than those without such alleles. However, the differences did not reach statistical significance in AD group. There was no correlation between acid-extractable A beta or insoluble A3 levels and the number of amyloid plaques in AD and control brains. However, insoluble A beta levels correlated positively with the number of NFT in AD brains. Our results show that although apoE epsilon 4 influences the accumulation of A beta, multiple processes may be involved in deposition of A beta in the brain.
