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The 129 codon polymorphism of the prion protein gene influences earlier cognitive performance in Down syndrome

Roberto Del Bo1, Giacomo Pietro Comi, Roberto Giorda

  • 1Dipartimento di Scienze Neurologiche, Padiglione Ponti, I. R. C. S. S. Ospedale Maggiore Policlinico, Via F. Sforza, 35, 20122 Milan, Italy. gpcomi@mailserver.unimi.it

Journal of Neurology
|June 11, 2003
PubMed

Insights

The prion protein gene (PRNP) polymorphism at codon 129 may accelerate cognitive decline in Down syndrome (DS) individuals. Carrying the V allele, particularly with APOE4, is linked to faster intellectual decline in DS patients.

Area of Science:

  • Neurogenetics
  • Gerontology
  • Developmental Disorders

Background:

  • Down syndrome (DS) is linked to intellectual disability and Alzheimer-like brain changes.
  • A common prion protein gene (PRNP) polymorphism (M129V) is associated with cognitive impairment in the elderly.
  • The role of PRNP M129V polymorphism in cognitive decline in DS patients is not well understood.

Purpose of the Study:

  • To investigate the association between the PRNP M129V polymorphism and cognitive decline in Italian Down syndrome patients.
  • To explore potential interactions between PRNP M129V and APOE epsilon 4 alleles regarding cognitive trajectory in DS.

Main Methods:

  • Genotyping of the PRNP codon 129 polymorphism in 122 Italian DS patients.
  • Assessment of allele frequencies in DS subjects compared to the general population.
  • Analysis of cognitive decline rates stratified by PRNP genotype and APOE status.

Main Results:

  • PRNP codon 129 allele frequencies in DS patients did not differ from the general population.
  • DS patients with at least one V allele showed a significantly faster rate of intellectual decline compared to M/M homozygotes.
  • An additive negative effect was observed for the apolipoprotein E epsilon 4 (APOE4) allele.

Conclusions:

  • PRNP gene variability at codon 129 may accelerate cognitive decline in Down syndrome.
  • The M129V polymorphism is a potential genetic modifier of cognitive trajectory in DS.
  • This genetic factor may contribute to earlier onset or faster progression of cognitive impairment in DS individuals.

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