Devi G, Fotiou A, Jyrinji D, Tycko B, DeArmand S, Rogaeva E, Song Y Q, Medieros H, Liang Y, Orlacchio A, Williamson J, St George-Hyslop P, Mayeux R
Taub Institute for Research on Alzheimer's Disease and the Aging Brain,The Gertrude Sergievsky Center, Columbia University, New York, NY 10032, USA.
Arch Neurol. 2000 Oct;57(10):1454-7. doi: 10.1001/archneur.57.10.1454.
Two children of an adult with early-onset, autopsy-confirmed Alzheimer disease (AD) developed dementia in their late 20s and were subsequently found to have novel mutations in codon 434 of the presenilin 1 (PS1) gene on chromosome 14, a G-to-T substitution at nucleotide 1548 and a C-to-G substitution at nucleotide 1549. The younger of the 2 children had AD confirmed at postmortem examination. The disease course in these 3 individuals was characterized by cognitive and behavioral problems accompanied by myoclonus, seizures, and aphasia within 5 years after onset. Two grandparents had clinically diagnosed AD with stroke beginning at ages 78 and 66 years, but neither had a PS1 mutation. No other living family member was demented, nor did any other family member have the PS1 mutation. We conclude that the affected parent of the proband was a likely recent founder for these novel mutations in PS1. The family demonstrates the clinical and genetic heterogeneity of AD. Arch Neurol. 2000;57:1454-1457