RGD Reference Report - Glutathione S-transferase P1 and T1 gene polymorphisms predict longitudinal course and age at onset of Alzheimer disease. - Rat Genome Database

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Glutathione S-transferase P1 and T1 gene polymorphisms predict longitudinal course and age at onset of Alzheimer disease.

Authors: Spalletta, G  Bernardini, S  Bellincampi, L  Federici, G  Trequattrini, A  Ciappi, F  Bria, P  Caltagirone, C  Bossu, P 
Citation: Spalletta G, etal., Am J Geriatr Psychiatry. 2007 Oct;15(10):879-87.
RGD ID: 5490271
Pubmed: PMID:17911365   (View Abstract at PubMed)
DOI: DOI:10.1097/JGP.0b013e3180547076   (Journal Full-text)

OBJECTIVE: Oxidative stress has been suggested as a contributor of Alzheimer disease (AD) neurodegeneration, particularly in those patients with late-onset AD (LOAD). Therefore, the authors studied the effect of glutathione S-transferase (GST) P1-M1-T1 gene polymorphisms and their interactions with the apolipoprotein E (ApoE) epsilon4 allelic variant on the three-year longitudinal course of AD. METHODS: Global cognitive level as measured by the Mini-Mental State Exam, basic activities of daily living (BADLs) as measured by the Physical Self-Maintenance Scale, and behavior as measured by the Neuropsychiatric Inventory, were assessed at baseline and after 1, 2, and 3 years in a sample of 99 LOAD patients. These subjects were drug naive and had undergone the first clinical examination for the diagnosis of AD. RESULTS: A multiple regression analysis indicated that the presence of ApoE epsilon4 allelic variant or GSTT1 null phenotype predicted the faster age at onset of the illness (F = 5.76, df = 2, 96, p = 0.0043). Carriers of GSTP1 *C allelic variant had a faster decline in cognitive functions (repeated measures analysis of variance [ANOVA]: F = 4.00, df = 3, 285, p = 0.008) and in BADLs (repeated measures ANOVA: F = 5.27, df = 3, 285, p = 0.001). This faster decline was independent from ApoE epsilon4 allele possession. No effect of GST P1-M1-T1 polymorphisms was found on behavioral symptom severity. CONCLUSION: These data are in line with the hypotheses that oxidative damage is a prominent feature in the clinical progression and the age at onset of LOAD.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Alzheimer's disease onsetIAGP 5490271DNA:polymorphism:exon:RGD 
Alzheimer's disease onsetIAGP 5490271DNA:deletion: :RGD 
Alzheimer's disease onsetISOGSTP1 (Homo sapiens)5490271; 5490271DNA:polymorphism:exon:RGD 
Alzheimer's disease onsetISOGSTT1 (Homo sapiens)5490271; 5490271DNA:deletion: :RGD 

Objects Annotated

Genes (Rattus norvegicus)
Gstp1  (glutathione S-transferase pi 1)
Gstt1  (glutathione S-transferase theta 1)

Genes (Mus musculus)
Gstp1  (glutathione S-transferase, pi 1)
Gstt1  (glutathione S-transferase, theta 1)

Genes (Homo sapiens)
GSTP1  (glutathione S-transferase pi 1)
GSTT1  (glutathione S-transferase theta 1)


Additional Information