What you carry at this position in your DNA and what research says about it.
Alzheimer's Disease Risk: 6/10 evidence, 51 publications.
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Sample genotype (not yours): T/T
Higher Risk of Alzheimer's and Cognitive Decline
Two copies of the T allele lead to reduced APOE gene expression. This reduction is associated with an increased risk of developing Alzheimer's disease and faster cognitive aging.
What this genotype means: Reduced APOE gene expression; Increased risk of Alzheimer's disease; Faster age-related cognitive decline.
Sample genotype (not yours): G/G
Lower Risk of Alzheimer's and Typical Cognitive Aging
Two copies of the G allele boost APOE gene expression, which helps protect the brain. This genotype is associated with a lower risk of Alzheimer's disease and more resilient cognitive aging.
What this genotype means: Increased APOE gene expression; Lower risk of Alzheimer's disease; More resilient cognitive aging.
Sample genotype (not yours): T/G
Slightly Increased Risk of Alzheimer's Disease
One copy of each allele represents an intermediate state for APOE gene expression. This genetic profile is linked to a slightly elevated risk of cognitive decline compared to the protective G/G genotype.
What this genotype means: Moderate APOE gene expression; Slightly increased risk of Alzheimer's disease; Intermediate cognitive aging profile.
Gene function and biological role
Gene Function: APOE encodes apolipoprotein E, a major cholesterol carrier in both the brain and the cardiovascular system [1]. This protein plays a critical role in clearing amyloid-beta plaques, which are a primary hallmark of Alzheimer's disease pathology [2]. Variations within this gene represent the most significant genetic risk factors for late-onset Alzheimer's disease identified to date [3]. Beyond its neurological functions, the protein is essential for transporting lipids and maintaining normal blood cholesterol levels [4].
Variant Impact: Located in the promoter region of the APOE gene, rs405509 directly regulates how much apolipoprotein E is produced by the body [5]. The T allele reduces transcriptional activity, leading to lower levels of the protective ApoE protein in the brain [6]. Conversely, the G allele increases promoter activity, boosting protein levels [7]. This regulatory change modifies the risk of neurodegeneration and cognitive decline, particularly when inherited alongside other APOE variants [8].
Key Insight: The G allele of this promoter variant can boost APOE gene transcription by over 160 percent compared to the T allele, significantly increasing the brain's protective ApoE protein levels.
Location: APOE. Chromosome 19 · 19q13.32 · 44.9 Mb
Estimated prevalence by population
Global 19.4%; European 22.8%; African 6.4%; East Asian 48.2%; South Asian 30.9%; Americas 24.8%; Ashkenazi 21.7%; Finnish 19.6%; Middle Eastern 25.7%; Amish 19.2%.
Estimated TT genotype frequency.
Global 46.3%; European 49.9%; African 37.8%; East Asian 42.4%; South Asian 49.4%; Americas 50.0%; Ashkenazi 49.8%; Finnish 49.4%; Middle Eastern 50.0%; Amish 49.2%.
Estimated TG genotype frequency.
Global 34.4%; European 27.3%; African 55.8%; East Asian 9.3%; South Asian 19.7%; Americas 25.2%; Ashkenazi 28.6%; Finnish 31.0%; Middle Eastern 24.3%; Amish 31.5%.
Estimated GG genotype frequency.
Showing effects for T/T genotype
Neurology & Mental Health
Neurodegenerative Diseases
Alzheimer's Disease. Evidence: 6/10. Source: PMID 30636644. Increased Risk.
Cognitive Performance
Cognitive Decline. Evidence: 6/10. Source: PMID 25085564. Faster Decline.
Cardiovascular & Metabolic
Lipids & Cholesterol
HDL Cholesterol. Evidence: 7/10. Source: PMID 31719535. Higher Levels.
Pharmacogenomics
Antidepressant & Psychiatric Drug Response
Antidepressant Response. Evidence: 5/10. Source: PMID 32795354. Better SSRI Response.
Anticoagulant & Blood Thinner Response
Warfarin Sensitivity. Evidence: 3/10. Source: PMID 33437219. Typical Sensitivity.
Showing effects for G/G genotype
Alzheimer's Disease. Evidence: 6/10. Source: PMID 30636644. Lower Risk.
Cognitive Decline. Evidence: 6/10. Source: PMID 25085564. More Resilient.
HDL Cholesterol. Evidence: 7/10. Source: PMID 31719535. Lower Levels.
Antidepressant Response. Evidence: 5/10. Source: PMID 32795354. Typical Response.
Warfarin Sensitivity. Evidence: 3/10. Source: PMID 33437219. Altered Sensitivity.
Showing effects for T/G genotype
Alzheimer's Disease. Evidence: 6/10. Source: PMID 30636644. Slightly Increased.
Cognitive Decline. Evidence: 6/10. Source: PMID 25085564. Intermediate.
HDL Cholesterol. Evidence: 7/10. Source: PMID 31719535. Typical Levels.
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
Inheriting two copies of the T allele significantly lowers the transcription of the APOE gene, resulting in fewer protective ApoE proteins in the brain [1]. This deficit impairs the clearance of amyloid-beta plaques, accelerating the onset of neurodegenerative processes [2]. Studies show that T/T homozygotes face a higher risk of late-onset Alzheimer's disease and exhibit more pronounced brain tissue atrophy with age [3]. Cognitive performance, particularly in memory and attention, tends to decline more rapidly in older adults with this genotype [4]. On the positive side, the T allele is associated with higher levels of beneficial HDL cholesterol [5]. Additionally, some research suggests that this genotype may correlate with a more favorable response to selective serotonin reuptake inhibitors (SSRIs) during depression treatment [6].
Reduced APOE gene expression; Increased risk of Alzheimer's disease; Faster age-related cognitive decline; Higher circulating HDL cholesterol levels.
Sample genotype: GG (Homozygous)
Two copies of the G allele significantly enhance the transcriptional activity of the APOE promoter, boosting protein levels [1]. Higher levels of ApoE protein facilitate efficient lipid transport and support the clearance of toxic amyloid-beta plaques in the brain [2]. Consequently, individuals with the G/G genotype experience a lower risk of late-onset Alzheimer's disease and a later average age of onset [3]. Brain imaging reveals better preservation of gray matter volume and healthier functional networks during normal aging [4]. While this genotype is highly protective for brain health, it is associated with slightly lower levels of beneficial HDL cholesterol [5]. There is also a potential association with altered sensitivity to certain medications like warfarin, though this effect is considered preliminary [6].
Increased APOE gene expression; Lower risk of Alzheimer's disease; More resilient cognitive aging; Slightly lower HDL cholesterol levels.
Sample genotype: TG (Heterozygous)
Possessing one copy of each allele results in moderate promoter activity and intermediate levels of ApoE protein expression [1]. The presence of the T allele slightly elevates the risk of developing Alzheimer's disease, particularly when other high-risk APOE variants are present [2]. Brain imaging studies of heterozygous individuals show intermediate patterns of age-related gray matter volume loss compared to the two homozygous groups [3]. Cognitive decline in memory and attention domains is typically less severe than in T/T carriers but more pronounced than in G/G carriers [4]. This genotype also exhibits intermediate levels of HDL cholesterol, balancing the lipid-raising effects of the T allele [5]. Overall, this genetic profile represents a common, middle-ground risk level for both cardiovascular and neurological outcomes.
Moderate APOE gene expression; Slightly increased risk of Alzheimer's disease; Intermediate cognitive aging profile.
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
Alzheimer's disease risk variants show association with cerebrospinal fluid amyloid beta.
Genome-wide analysis of genetic predisposition to Alzheimer's disease and related sex disparities.
Content updated August 2026.
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