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<EM>SLC2A1</EM> RS841847 T ALLELE REDUCES THE RISK FOR LATE-ONSET ALZHEIMER'S DISEASE
Agnes Feherand 4 co-authors
University of Szeged
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS05-09AM-205
Presentation
Date TBA
Board: PS05-09AM-205
Event Information
Poster Board
PS05-09AM-205
Poster
View posterAbstract
Alzheimer’s disease (AD) and type-2 diabetes mellitus share overlapping pathophysiological mechanisms, including impaired glucose metabolism. Glucose transporter 1 (GLUT1), encoded by the SLC2A1 gene, regulates cerebral glucose uptake across the blood-brain barrier and has been shown to be altered in AD. The SLC2A1 rs841847 C>T polymorphism has been associated with type-2 diabetes, but its role in AD has not been investigated.
We conducted a case-control study including 439 non-diabetic patients with late-onset AD (mean age±SD: 74.5±6.6 years; 34.9% male) and 304 cognitively healthy, age-matched controls (74.8±7.1 years; 36.0% male). We examined the impact of the Apolipoprotein E (APOE) ε4 allele, a well-characterized genetic risk factor for AD, as previous reports indicate that ε4 allele carriers display upregulation of GLUT1. Genotyping of SLC2A1 and APOE polymorphisms was performed using TaqMan assays.
The T allele was significantly more frequent in the control group than in AD patients, and its presence was associated with reduced risk for AD relative to the C/C genotype (T: AD 22.8%, controls 28.1%; OR=0.674; p=0.009). The ε4 allele was significantly over-represented in AD (ε4: AD: 27.2%, control: 10.5%; p<0.001). No interaction was detected between the two polymorphisms on AD risk.
These findings indicate a moderate protective effect for the rs841847 variant allele in AD, which is consistent with the suggested role of altered GLUT1-mediated glucose homeostasis in AD pathophysiology. Our results suggest the rs841847 polymorphism as a candidate polymorphism for further study, and may contribute to future meta-analyses.
We conducted a case-control study including 439 non-diabetic patients with late-onset AD (mean age±SD: 74.5±6.6 years; 34.9% male) and 304 cognitively healthy, age-matched controls (74.8±7.1 years; 36.0% male). We examined the impact of the Apolipoprotein E (APOE) ε4 allele, a well-characterized genetic risk factor for AD, as previous reports indicate that ε4 allele carriers display upregulation of GLUT1. Genotyping of SLC2A1 and APOE polymorphisms was performed using TaqMan assays.
The T allele was significantly more frequent in the control group than in AD patients, and its presence was associated with reduced risk for AD relative to the C/C genotype (T: AD 22.8%, controls 28.1%; OR=0.674; p=0.009). The ε4 allele was significantly over-represented in AD (ε4: AD: 27.2%, control: 10.5%; p<0.001). No interaction was detected between the two polymorphisms on AD risk.
These findings indicate a moderate protective effect for the rs841847 variant allele in AD, which is consistent with the suggested role of altered GLUT1-mediated glucose homeostasis in AD pathophysiology. Our results suggest the rs841847 polymorphism as a candidate polymorphism for further study, and may contribute to future meta-analyses.
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