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J Neurol Neurosurg Psychiatry 2002;72:732-736 doi:10.1136/jnnp.72.6.732
  • Paper

Lipoprotein(a), apolipoprotein E genotype, and risk of Alzheimer's disease

  1. V Solfrizzi,
  2. F Panza,
  3. A D'Introno,
  4. A M Colacicco,
  5. C Capurso,
  6. A M Basile,
  7. A Capurso
  1. Department of Geriatrics, Centre for Aging Brain, Memory Unit, University of Bari, Policlinico, Piazza Giulio Cesare 11, 70124 Bari, Italy
  1. Correspondence to:
 Dr A Capurso, Department of Geriatrics, Centre for Aging Brain, Memory Unit, University of Bari, Policlinico, Piazza Giulio Cesare 11, 70124 Bari, Italy;
 a.capurso{at}geriatria.uniba.it or Dr Vincenzo Solfrizzi;
 geriat.dot{at}geriatria.uniba.it
  • Received 19 October 2001
  • Accepted 13 February 2002
  • Revised 1 February 2002

Abstract

Objectives: To explore the possible role of serum lipoprotein(a) (Lp(a)), apolipoprotein E polymorphism, and total cholesterol (TC) serum concentrations in Alzheimer's disease (AD).

Methods: Lp(a) serum concentrations, apolipoprotein E genotypes, and TC serum concentrations were determined in 61 patients with a diagnosis of probable AD and in 63 healthy unrelated age matched controls. Genomic DNA was obtained and amplified by polymerase chain reaction and apolipoprotein E genotypes were defined following a previously described procedure.

Results: Lp(a) serum concentrations were significantly associated in a non-linear relation with an increased risk for AD, independently of apolipoprotein E genotypes and sex and dependent on age (truth association) and TC serum concentrations (spurious association). The effect of age adjusted for TC on the odds of having AD increased non-linearly with increasing Lp(a) serum concentrations, with a plateau between 70 and 355 mg/l (odds ratio 11.33). For Lp(a) serum concentrations ≥ 360 mg/l, the effect of age (≥ 72 years) was associated with a reduction in odds of having AD (odds ratio 0.15).

Conclusion: It is suggested that increased Lp(a) serum concentrations, by increasing the risk for cerebrovascular disease, may have a role in determining clinical AD.

Footnotes

  • Competing interests: none declared.

  • Previously presented at the 7th international conference on Alzheimer's disease and related disorders, 9–13 July 2000, Washington DC, USA.

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