What you carry at this position in your DNA and what research says about it.
Alzheimer's Disease Risk: 8/10 evidence, 16 publications.
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Sample genotype (not yours): C/C
Typical Alzheimer's Risk and Better Cognitive Performance
Inheriting two copies of the protective C allele is linked to a lower risk of cognitive decline. This genotype is also associated with healthier triglyceride profiles.
What this genotype means: Lower risk of late-onset Alzheimer's disease; Better cognitive performance in older age; Favorable blood triglyceride levels.
Sample genotype (not yours): C/G
Moderately Increased Risk of Alzheimer's Disease
Carrying one copy of the G risk allele is associated with a moderate increase in the risk of cognitive decline. It also correlates with slightly higher triglyceride levels.
What this genotype means: Moderately elevated risk of late-onset Alzheimer's; Potential for slightly faster memory decline in older age; Slightly higher circulating triglyceride levels.
Sample genotype (not yours): G/G
Higher Risk of Alzheimer's Disease and Cognitive Decline
Two copies of the G allele are linked to a significantly higher risk of Alzheimer's disease. This genotype is also associated with poorer late-life cognitive function and elevated triglycerides.
What this genotype means: Significantly higher risk of late-onset Alzheimer's disease; Increased rate of cognitive and memory decline in later life; Elevated blood triglyceride levels.
Gene function and biological role
Gene Function: The APOE gene encodes apolipoprotein E, a major cholesterol-carrying protein in the brain and peripheral tissues [1]. It plays a critical role in lipid transport, cellular repair, and the clearance of amyloid-beta plaques [2]. Variations in this gene are the most significant genetic risk factors for late-onset Alzheimer's disease [3]. Beyond neurodegenerative risk, APOE is heavily involved in cardiovascular health and lipid metabolism [4].
Variant Impact: Located in the first intron of the APOE gene, rs440446 is a common single nucleotide variant also known as the IVS1+69 or +113G/C polymorphism [5]. Although it does not directly alter the amino acid sequence of the main apolipoprotein E protein, it resides in an enhancer region and is thought to influence transcriptional efficiency [1]. This variant is in strong linkage disequilibrium with the well-known APOE epsilon alleles, meaning it is frequently inherited alongside them and serves as a strong proxy for Alzheimer's risk [2]. It is also associated with differences in cognitive performance and circulating lipid levels [6].
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Key Insight: This variant is located in an intron but acts as a powerful genetic proxy for the APOE epsilon 4 risk state. The G allele is strongly linked to higher Alzheimer's risk, while the C allele is protective.
Location: APOE. Chromosome 19 · 19q13.32 · 44.9 Mb
Estimated prevalence by population
Global 11.1%; European 13.1%; African 2.0%; East Asian 35.0%; South Asian 22.9%; Americas 16.8%; Ashkenazi 14.3%; Finnish 7.0%; Middle Eastern 23.0%; Amish 9.2%.
Estimated CC genotype frequency.
Global 40.1%; European 46.2%; African 24.5%; East Asian 48.3%; South Asian 49.9%; Americas 48.4%; Ashkenazi 47.0%; Finnish 39.0%; Middle Eastern 49.9%; Amish 42.3%.
Estimated CG genotype frequency.
Global 48.7%; European 40.7%; African 73.5%; East Asian 16.7%; South Asian 27.1%; Americas 34.9%; Ashkenazi 38.7%; Finnish 53.9%; Middle Eastern 27.1%; Amish 48.5%.
Estimated GG genotype frequency.
Showing effects for C/C genotype
Neurology & Mental Health
Neurodegenerative Diseases
Alzheimer's Disease. Evidence: 8/10. Source: PMID 30979435. Typical Risk.
Cognitive Performance
Cognitive Function. Evidence: 6/10. Source: PMID 40374629. Better Function.
Cardiovascular & Metabolic
Lipids & Cholesterol
Triglycerides. Evidence: 4/10. Source: PMID 37821706. Typical Levels.
Blood Cell & Iron Traits
Eosinophil Count. Evidence: 7/10. Source: PMID 30595370. Higher Count.
Showing effects for C/G genotype
Alzheimer's Disease. Evidence: 8/10. Source: PMID 30979435. Increased Risk.
Cognitive Function. Evidence: 6/10. Source: PMID 40374629. Typical.
Triglycerides. Evidence: 4/10. Source: PMID 37821706. Slightly Elevated.
Eosinophil Count. Evidence: 7/10. Source: PMID 30595370. Typical.
Showing effects for G/G genotype
Alzheimer's Disease. Evidence: 8/10. Source: PMID 30979435. ~1.6x Higher Risk.
Cognitive Function. Evidence: 6/10. Source: PMID 40374629. Poorer Function.
Triglycerides. Evidence: 4/10. Source: PMID 37821706. Elevated Levels.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
A double dose of the C allele is highly protective against late-onset neurodegenerative conditions. Large-scale genomic studies demonstrate that this genotype is associated with a significantly lower risk of developing Alzheimer's disease compared to G allele carriers [1]. Cognitive assessments in older cohorts show that this genetic profile supports better overall cognitive function and memory performance in later life [2]. Lipid metabolism is also optimized, with studies indicating lower circulating triglyceride levels [3]. Additionally, some research suggests a slight elevation in eosinophil counts, though this remains within normal physiological ranges [4].
Lower risk of late-onset Alzheimer's disease; Better cognitive performance in older age; Favorable blood triglyceride levels.
Sample genotype: CG (Heterozygous)
Possessing one copy of the G allele introduces a moderate genetic predisposition to cognitive decline. Research indicates that this heterozygous state elevates the risk of late-onset Alzheimer's disease compared to the protective C/C genotype [1]. This risk is largely driven by the strong linkage between the G allele and the APOE epsilon 4 isoform [2]. While cognitive performance in mid-life remains typical, older age may bring a slightly faster rate of memory decline [3]. Metabolic profiles may also show a mild elevation in circulating triglycerides, requiring standard cardiovascular monitoring [4].
Moderately elevated risk of late-onset Alzheimer's; Potential for slightly faster memory decline in older age; Slightly higher circulating triglyceride levels.
Sample genotype: GG (Homozygous)
Carrying two copies of the G allele represents a notable genetic risk factor for neurodegenerative disease. Multiple genome-wide association studies confirm a strong link between this genotype and an increased risk of late-onset Alzheimer's disease [1]. This association is primarily a consequence of the variant's tight genetic linkage to the high-risk APOE epsilon 4 allele [2]. Longitudinal studies of older adults show a more pronounced decline in memory and general cognitive performance over time [3]. Furthermore, metabolic assessments show a clear association with elevated blood triglyceride levels, which can impact overall cardiovascular health [4].
Significantly higher risk of late-onset Alzheimer's disease; Increased rate of cognitive and memory decline in later life; Elevated blood triglyceride levels.
Variants with shared genetic architecture
rs429358 · APOE Gene · Chr 19 · Alzheimer's Disease Risk
rs7412 · APOE Gene · Chr 19 · Cholesterol and Heart Risk
rs769449 · APOE Gene · Chr 19 · Alzheimer's Disease Risk
Similar Genetic Architecture of Alzheimer's Disease and Differential APOE Effect Between Sexes.
Identification of genetic heterogeneity of Alzheimer's disease across age.
The APOE -219G/T and +113G/C polymorphisms affect insulin resistance among Turks.
Mexican Biobank advances population and medical genomics of diverse ancestries.
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
Sex-specific genetic architecture of late-life memory performance.
Content updated August 2026.
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