Glutathione S-Transferase P1 and T1 Gene Polymorphisms Predict Longitudinal Course and Age at Onset of Alzheimer Disease

GSTM1 null genotype as risk factor for late-onset Alzheimer's disease in Italian patients

“…Some studies have investigated the association among GST genes and AD risk with conflicting findings, but none of these studies have observed a significant association between the GSTM1 null genotype and AD risk [12,13,[22][23][24][25]. Our study suggests that the GSTM1 null genotype is a risk factor for AD in an Italian study population.…”

“…Over the last two decades, a significant body of data has been accumulated linking genetic variability of GSTs with the development and expression of several multifactorial diseases [19][20][21]. To date some studies have been conducted on GST gene variability in AD [12,13,[22][23][24][25]. However, the results of these studies are in some cases conflicting and insufficient to clarify the role of GST genes in AD.…”

Oxidative Stress and β-Amyloid Protein in Alzheimer’s Disease

“…Moreover, Butterfield's laboratory identified 16 oxidized proteins that were oxidatively modified and involved in energy metabolism, proteasome function, and scavenging of oxidants (Boyd-Kimball et al 2006). Many of these oxidized proteins are also represented in AD brain (BoydKimball et al 2006), including ATP synthase a chain (Butterfield and Lauderback 2002;Sergeant et al 2003), glutamate dehydrogenase (Blass and Gibson 1991), proteasome a and b subunit (Zouambia et al 2008), glutathione S-transferase (Li et al 2006;Spalletta et al 2007), myosin regulatory light chain (Frackowiak et al 1994), adenosine kinase (Lee et al 1997), malate dehydrogenase (Op den Velde and Stam 1976), transketolase (Paoletti et al 1997;Tombaccini et al 1994), translation elongation factor EF-1c (Li et al 2005;Reed et al 2008), lipidbinding protein (Chang et al 2005;Hirsch-Reinshagen et al 2009), and receptors for activated C kinase (Battaini et al 1999;Shimohama et al 1998). It was also reported that oxidative stress in brain of Alzheimer transgenic mice requires the presence of a single methionine residue at position 35 of the Ab because all indices of oxidative damage in brain were completely prevented in genetically and age-matched APP mice with an M631L mutation in APP (Butterfield et al 2010a;Kanski et al 2002).…”

Efficacy of a Vitamin/Nutriceutical Formulation for Early-stage Alzheimer's Disease: A 1-year, Open-label Pilot Study With an 16-Month Caregiver Extension

“…22,23 Polymorphisms of this enzyme with diminished activity potentiate the impact of apolipoprotein E (ApoE) deficiency. 24,25 Strategies to maintain appropriate GSH production may be useful as part of a therapeutic approach to delay the onset or progression of AD. Glutathione itself cannot be taken up; however, the GSH precursor N-acetyl cysteine (NAC) increases GSH production, and demonstrated some efficacy in clinical trials.…”