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Clinical Chemistry 51: 944-951, 2005. First published April 1, 2005; 10.1373/clinchem.2004.045955
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(Clinical Chemistry. 2005;51:944-951.)
© 2005 American Association for Clinical Chemistry, Inc.

Molecular Diagnostics and Genetics

Glutathione S-Transferase P1 *C Allelic Variant Increases Susceptibility for Late-Onset Alzheimer Disease: Association Study and Relationship with Apolipoprotein E {epsilon}4 Allele

Sergio Bernardini1,a, Lorenza Bellincampi1, Sabrina Ballerini1, Giorgio Federici1,2, Roberta Iori1, Alberto Trequattrini3, Fabrizio Ciappi3, Francesca Baldinetti4, Paola Bossù4, Carlo Caltagirone4,5 and Gianfranco Spalletta4,5

1 Departments of Internal Medicine and Laboratory Medicine-PTV, and 5 Department of Neuroscience, University of Rome "Tor Vergata", Rome, Italy.
2 Bambino Gesù-Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Hospital, Rome, Italy.
3 ASL Città di Castello, Perugia, Italy.
4 Istituto di Ricovero e Cura a Carattere Scientifico Fondazione Santa Lucia, Rome, Italy.

aAddress correspondence to this author at: Department of Internal Medicine, University of Rome "Tor Vergata", Via Montpellier 1, 00133 Rome, Italy. Fax 39-06-20902357; e-mail Bernardini{at}Med.UniRoma2.it.

Background: Oxidative stress and neuronal cell death have been implicated in the pathogenesis of Alzheimer disease (AD). Considering that the glutathione transferase (GST) supergene family encodes isoenzymes that appear to be critical in protection against oxidative stress, we aimed at determining the various GSTP1, GSTM1, and GSTT1 polymorphisms and ApoE genotypes to investigate their role as susceptibility genes for late-onset AD (LOAD).

Methods: We included 210 LOAD patients and 228 healthy controls matched for age, sex, and educational level in our case–control genetic association study. GSTM1 and GSTT1 genotypes were studied by conventional PCR, whereas GSTP1 and ApoE genotypes were determined by real-time PCR on the LightCycler.

Results: We found a significant association between LOAD and the GSTP1*C allelic variant [odds ratio (OR) = 1.9; P <0.05], but no association between the GSTM1 and GSTT1 deleted genotypes and LOAD. In addition, a preliminary result suggested that carriers of both the GSTP1*C and ApoE {epsilon}4 allelic variants were at increased risk of LOAD (OR = 19.98; P <0.0001).

Conclusion: The GSTP1*C allelic variant should be considered a candidate for LOAD, particularly in persons having the ApoE {epsilon}4 allelic variant, because the GSTP1 and ApoE gene products are implicated in oxidative stress and apoptosis processes leading to ß-amyloid-mediated neurodegeneration.




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