What you carry at this position in your DNA and what research says about it.
Alzheimer's Disease Risk: 10/10 evidence, 18 publications.
You're viewing every possible genotype for this variant.
None of these is your result. Use the genotype toggle to compare them, then sign up and upload your DNA to see which one is yours.
Sample genotype (not yours): C/C
Typical Alzheimer's Risk
Two copies of the protective C allele are associated with a typical risk of developing Alzheimer's disease. This genetic profile does not carry the elevated risk associated with the T allele.
What this genotype means: Typical baseline risk for Alzheimer's disease; Typical memory and language performance during aging.
Sample genotype (not yours): C/T
Increased Alzheimer's Risk
One copy of the T allele is associated with a moderately increased risk of developing Alzheimer's disease. It is also linked to slightly faster cognitive decline in late life.
What this genotype means: Moderately increased risk of Alzheimer's disease; Slightly faster cognitive decline during aging.
Sample genotype (not yours): T/T
Elevated Alzheimer's Risk
Two copies of the T allele are associated with the highest genetic risk at this locus for Alzheimer's disease. It is also linked to earlier onset of cognitive symptoms.
What this genotype means: Significantly increased risk of Alzheimer's disease; Earlier onset of cognitive symptoms.
Gene function and biological role
Gene Function: BIN1 encodes the bridging integrator 1 protein, which is the second most important genetic risk factor for late-onset Alzheimer's disease after APOE [1]. This protein is heavily involved in endocytosis, membrane trafficking, and cytoskeletal regulation within brain cells [2]. Research indicates that BIN1 interacts directly with tau protein, a key driver of neurofibrillary tangles in Alzheimer's pathology [3]. It is also highly expressed in microglia, the brain's resident immune cells, where it plays a critical role in regulating neuroinflammation [4].
Variant Impact: Located in an intron of the BIN1 gene region, rs6733839 acts as a major regulatory switch [1]. The risk-associated T allele alters a binding site for the transcription factor MEF2C, which specifically increases BIN1 expression in microglia [4]. This elevated expression is thought to disrupt normal endocytosis and promote the accumulation of toxic proteins in the brain [3]. Consequently, this variant is strongly associated with increased susceptibility to late-onset Alzheimer's disease and accelerated cognitive decline [2].
Key Insight: BIN1 is the second most significant genetic risk factor for late-onset Alzheimer's disease, and this specific variant alters microglia immune cell behavior in the brain.
Location: BIN1. Chromosome 2 · 2q14.3 · 127.1 Mb
Estimated prevalence by population
Global 36.8%; European 37.8%; African 36.5%; East Asian 36.2%; South Asian 36.1%; Americas 31.4%; Ashkenazi 39.3%; Finnish 38.5%; Middle Eastern 49.6%; Amish 31.6%.
Estimated CC genotype frequency.
Global 47.7%; European 47.4%; African 47.8%; East Asian 47.9%; South Asian 48.0%; Americas 49.3%; Ashkenazi 46.8%; Finnish 47.1%; Middle Eastern 41.7%; Amish 49.2%.
Estimated CT genotype frequency.
Global 15.5%; European 14.8%; African 15.7%; East Asian 15.9%; South Asian 15.9%; Americas 19.3%; Ashkenazi 13.9%; Finnish 14.4%; Middle Eastern 8.8%; Amish 19.1%.
Estimated TT genotype frequency.
Showing effects for C/C genotype
Neurology & Mental Health
Neurodegenerative Diseases
Alzheimer's Disease. Evidence: 10/10. Source: PMID 24162737. Typical Risk.
Lewy Body Dementia. Evidence: 6/10. Source: PMID 33589841. Typical Risk.
Age of Alzheimer's Onset. Evidence: 10/10. Source: PMID 40883957. Typical Age.
Alzheimer's Pathology. Evidence: 3/10. Source: PMID 29458411. Typical Levels.
Memory, Learning & Attention
Memory Performance. Evidence: 7/10. Source: PMID 37349795. Typical Performance.
Cognitive Performance
Language Ability. Evidence: 6/10. Source: PMID 37349795. Typical Ability.
Showing effects for C/T genotype
Alzheimer's Disease. Evidence: 10/10. Source: PMID 24162737. ~1.18x Increased Risk.
Lewy Body Dementia. Evidence: 6/10. Source: PMID 33589841. ~1.16x Increased Risk.
Age of Alzheimer's Onset. Evidence: 10/10. Source: PMID 40883957. Slightly Earlier.
Alzheimer's Pathology. Evidence: 3/10. Source: PMID 29458411. Slightly Increased.
Memory Performance. Evidence: 7/10. Source: PMID 37349795. Slightly Lower.
Language Ability. Evidence: 6/10. Source: PMID 37349795. Slightly Lower.
Showing effects for T/T genotype
Alzheimer's Disease. Evidence: 10/10. Source: PMID 24162737. ~1.4x Increased Risk.
Lewy Body Dementia. Evidence: 6/10. Source: PMID 33589841. ~1.35x Increased Risk.
Age of Alzheimer's Onset. Evidence: 10/10. Source: PMID 40883957. Earlier Onset.
Alzheimer's Pathology. Evidence: 3/10. Source: PMID 29458411. Increased Levels.
Memory Performance. Evidence: 7/10. Source: PMID 37349795. Lower Performance.
Language Ability. Evidence: 6/10. Source: PMID 37349795. Lower Performance.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Two copies of the protective C allele are associated with typical baseline risk for late-onset Alzheimer's disease [1]. This genetic profile is linked to typical rates of cognitive aging, including stable memory performance and language ability over time [2]. Neuropathological studies indicate that this genotype is associated with lower levels of neuritic plaques and neurofibrillary tangles compared to T allele carriers [3]. Additionally, it is associated with a typical age of onset for age-related cognitive changes [4]. The C/C genotype represents the most common genetic baseline in the population.
Typical baseline risk for Alzheimer's disease; Typical memory and language performance during aging.
Sample genotype: CT (Heterozygous)
One copy of the T allele at this locus is associated with a moderately increased risk of late-onset Alzheimer's disease, with an odds ratio of approximately 1.18 [1]. This genetic variant is also linked to a higher risk of Lewy body dementia, suggesting a shared pathway in neurodegenerative diseases [2]. Research indicates that carriers of the T allele may experience slightly faster declines in episodic memory and language performance during aging [3]. On a cellular level, this variant is associated with a higher burden of neuritic plaques and neurofibrillary tangles in the brain [4]. These changes are thought to be driven by altered expression of the BIN1 protein in microglia [5].
Moderately increased risk of Alzheimer's disease; Slightly faster cognitive decline during aging.
Sample genotype: TT (Homozygous)
Two copies of the T allele are associated with the highest risk of developing Alzheimer's disease at this locus, with a significantly elevated odds ratio [1]. This genotype is also linked to an earlier age of onset for Alzheimer's symptoms compared to those with the protective C allele [2]. Cognitive studies show that individuals with the T/T genotype perform worse on tests of episodic memory and language ability in late life [3]. Neuropathological evaluations have found that this genotype correlates with the highest density of neuritic plaques and neurofibrillary tangles [4]. The T allele is believed to increase BIN1 protein levels, which disrupts cellular clearance mechanisms in the brain [5].
Significantly increased risk of Alzheimer's disease; Earlier onset of cognitive symptoms.
Variants with shared genetic architecture
rs744373 · BIN1 Gene · Chr 2 · Alzheimer's Disease Risk
rs7561528 · BIN1 Gene · Chr 2 · Alzheimer Disease Risk
rs769449 · APOE Gene · Chr 19 · Alzheimer's Disease Risk
Meta-analysis of 74,046 individuals identifies 11 new susceptibility loci for Alzheimer's disease.
Genome-wide pleiotropy analysis of neuropathological traits related to Alzheimer's disease.
A genome-wide association study of serum proteins reveals shared loci with common diseases.
Content updated August 2026.
ReadYourDNA provides educational interpretation of DNA data you already have. It is not diagnostic, not a substitute for professional medical advice, diagnosis, or treatment, and is not intended to diagnose, treat, cure, or prevent any disease. Talk to a clinician before acting on any result.
Raw DNA Data Reports for 23andMe & AncestryDNA · About ReadYourDNA · FAQ · Methodology & Science · Pricing · Support and complaints · Legal & Contact · Health Traits · Pharmacogenomics · Carrier Status · Variant Explorer · The Human Karyotype · Privacy Policy · Terms of Service · Accessibility · Consumer Health Data Privacy · Your Privacy Choices · Editorial Standards · Your Data, Checkable · Sample Report · ReadYourDNA and Promethease compared · What is inside a 23andMe raw data file · What is inside an AncestryDNA raw data file · What a chatbot can and cannot do with your raw DNA file · Where a raw DNA file can still be uploaded in 2026
Written, maintained and operated by Martin Pechhacker, sole proprietor, Vienna, Austria. Trade register GISA 40064420. support@readyourdna.com