Journal of Neural Transmission - Parkinson's Disease and Dementia Section

, Volume 5, Issue 1, pp 63–65

Sequencing of exons 16 and 17 of the β-amyloid precursor protein gene reveals the β-amyloid sequence to be normal in cases of the parkinson dementia complex of guam

Authors

  • M. -C. Chartier Harlin
    • Alzheimer's Disease Research Group, Departments of Biochemistry and Molecular GeneticsSt. Mary's Hospital Medicial School
  • F. Crawford
    • Alzheimer's Disease Research Group, Departments of Biochemistry and Molecular GeneticsSt. Mary's Hospital Medicial School
  • D. P. Perl
    • Neuropathology DivisionMt. Sinai Medical Center
  • J. Steele
    • Guam Memorial Hospital
  • J. Hardy
    • Alzheimer's Disease Research Group, Departments of Biochemistry and Molecular GeneticsSt. Mary's Hospital Medicial School
Short Communication

DOI: 10.1007/BF02260915

Cite this article as:
Chartier Harlin, M.-., Crawford, F., Perl, D.P. et al. J Neural Transm Gen Sect (1993) 5: 63. doi:10.1007/BF02260915

Summary

Exons 16 and 17 of the β-amyloid precursor protein gene has been sequenced in individuals with the amyotropic lateral sclerosis/Parkinson's dementia complex of Guam to test the hypothesis that this disease is an allelic variant of Alzheimer's disease and to test whether sequence differences within β-amyloid in this population contributes to the non-deposition of this peptide in the disorder. The sequence was normal.

Keywords

β-amyloidAPPamyotrophic lateral sclerosisParkinson's diseaseGuamgeneticsAlzheimer's disease
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Copyright information

© Springer-Verlag 1993