Novel presenilin 1 mutations associated with early onset of dementia in a family with both early-onset and late-onset Alzheimer disease

Arch Neurol. 2000 Oct;57(10):1454-7. doi: 10.1001/archneur.57.10.1454.

Abstract

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

Publication types

  • Case Reports
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adult
  • Age Distribution
  • Age of Onset
  • Aged
  • Alzheimer Disease / epidemiology
  • Alzheimer Disease / genetics*
  • Alzheimer Disease / metabolism
  • Apolipoproteins E / metabolism
  • Chromosome Aberrations / genetics
  • Chromosome Disorders
  • Chromosomes, Human, Pair 14 / genetics
  • Codon / genetics
  • DNA Mutational Analysis
  • Female
  • Humans
  • Male
  • Membrane Proteins / genetics*
  • Neurofibrillary Tangles / metabolism
  • Pedigree
  • Point Mutation / genetics*
  • Presenilin-1

Substances

  • Apolipoproteins E
  • Codon
  • Membrane Proteins
  • PSEN1 protein, human
  • Presenilin-1