Novel presenilin 1 mutation (S170F) causing Alzheimer disease with Lewy bodies in the third decade of life

Arch Neurol. 2005 Dec;62(12):1821-30. doi: 10.1001/archneur.62.12.1821.

Abstract

Background: Cases of early-onset Alzheimer disease (AD) with an autosomal dominant inheritance pattern (familial AD [FAD]) are rare but have greatly advanced our understanding of the molecular pathogenesis of AD. We describe herein a kindred with very early-onset FAD (age, <40 years) with unusual pathological features and a novel mutation in the presenilin 1 (PSEN1) gene (S170F) and review the existing literature on very early-onset FAD.

Objective: To analyze the neuropathological and genetic features of a family with onset of AD in the third decade of life.

Design, setting, and participants: The proband underwent full clinical assessment and postmortem examination at the Washington University Alzheimer's Disease Research Center, St Louis, Mo. Limited pathological samples and autopsy records of 2 affected family members were available. The proband underwent screening for mutations in genes linked with FAD.

Results: Dementia developed in 3 family members in this kindred at a mean age of 27 years; the proband had myoclonus, seizures, and rigidity, similar to findings in previously described kindreds with PSEN1 mutations. All 3 family members were confirmed to have AD by neuropathological examination. The proband also had widespread Lewy body pathology in the brainstem, limbic areas, and neocortex; specific staining for Lewy bodies was not performed in the other 2 family members. The proband had a single mutation (S170F) in exon 6 of the PSEN1 gene, which segregates with disease.

Conclusions: A novel PSEN1 mutation causes very-early-onset FAD with associated Lewy bodies. To our knowledge, this kindred has the earliest reported onset of pathologically confirmed FAD and dementia with Lewy bodies.

Publication types

  • Case Reports
  • Research Support, N.I.H., Extramural

MeSH terms

  • Adult
  • Age of Onset
  • Alzheimer Disease / genetics*
  • Alzheimer Disease / pathology
  • Alzheimer Disease / physiopathology
  • Amino Acid Substitution / genetics
  • Brain / metabolism
  • Brain / pathology
  • Brain / physiopathology
  • Chromosome Disorders / genetics
  • Chromosome Disorders / pathology
  • Chromosome Disorders / physiopathology
  • Disease Progression
  • Exons / genetics
  • Family Health
  • Fatal Outcome
  • Female
  • Genetic Predisposition to Disease / genetics*
  • Humans
  • Lewy Bodies / genetics*
  • Lewy Bodies / metabolism
  • Lewy Body Disease / genetics*
  • Lewy Body Disease / pathology
  • Lewy Body Disease / physiopathology
  • Male
  • Membrane Proteins / genetics*
  • Mutation / genetics*
  • Neurofibrillary Tangles / genetics
  • Neurofibrillary Tangles / metabolism
  • Neurofibrillary Tangles / pathology
  • Pedigree
  • Plaque, Amyloid / genetics
  • Plaque, Amyloid / metabolism
  • Plaque, Amyloid / pathology
  • Presenilin-1
  • alpha-Synuclein / genetics
  • alpha-Synuclein / metabolism

Substances

  • Membrane Proteins
  • PSEN1 protein, human
  • Presenilin-1
  • alpha-Synuclein