What you carry at this position in your DNA and what research says about it.
Dopamine and Addiction Risk: 5/10 evidence, 24 publications.
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Sample genotype (not yours): C/C
Typical Dopamine Regulation and Baseline Addiction Risk
Presence of the common C allele is associated with typical splicing of the dopamine D2 receptor. This results in a balanced ratio of receptor isoforms and standard baseline risks for substance dependence.
What this genotype means: Typical dopamine receptor splicing; Baseline risk for substance dependence; Standard working memory processing.
Sample genotype (not yours): A/A
Increased Addiction Risk and Altered Working Memory Processing
Two copies of the A allele are associated with a more pronounced shift in dopamine receptor splicing, increasing the risk for substance dependence.
What this genotype means: Reduced presynaptic D2S autoreceptor expression; Increased risk of substance dependence; Altered working memory and cognitive processing.
Sample genotype (not yours): C/A
Slightly Increased Addiction Risk and Altered Dopamine Splicing
A single copy of the A allele is linked to a shift in dopamine receptor splicing, which slightly increases the risk for alcohol and opioid dependence.
What this genotype means: Altered dopamine receptor isoform ratio; Slightly increased risk of alcohol and opioid dependence; Potential for better response to olanzapine.
Gene function and biological role
Gene Function: The DRD2 gene encodes the dopamine receptor D2, a key protein involved in the brain's reward, motivation, and cognitive control pathways [1]. This receptor is highly expressed in the striatum and prefrontal cortex, where it modulates synaptic dopamine availability [1]. DRD2 undergoes alternative splicing to produce two distinct isoforms: a short presynaptic form (D2S) and a long postsynaptic form (D2L) [2]. The short isoform acts primarily as an autoreceptor, regulating the release of dopamine into the synapse [2]. Proper balance between these two isoforms is essential for maintaining harmonious communication between dopamine, GABA, and glutamate systems [2].
Variant Impact: The rs1076560 variant is located within intron 6 of the DRD2 gene [1]. This specific genetic change acts as a splicing regulator, directly altering the ratio of the D2S and D2L receptor isoforms [1]. Specifically, the minor A allele is associated with decreased expression of the short presynaptic D2S isoform relative to the long postsynaptic D2L isoform [1]. This shift in isoform balance reduces the brain's ability to regulate dopamine release, leading to altered signaling in fronto-striatal circuits [1]. Consequently, this variant has been extensively studied for its impact on cognitive control, working memory, and susceptibility to substance dependence [2].
Key Insight: This variant acts as a molecular volume dial, shifting the balance between two different forms of the same dopamine receptor in the brain.
Location: DRD2. Chromosome 11 · 11q23.2 · 113.4 Mb
Estimated prevalence by population
Global 70.2%; European 70.8%; African 83.0%; East Asian 34.2%; South Asian 54.1%; Americas 53.0%; Ashkenazi 78.2%; Finnish 62.1%; Middle Eastern 83.1%; Amish 81.6%.
Estimated CC genotype frequency.
Global 26.5%; European 26.7%; African 16.2%; East Asian 48.6%; South Asian 38.9%; Americas 39.6%; Ashkenazi 20.5%; Finnish 33.4%; Middle Eastern 16.1%; Amish 17.4%.
Estimated CA genotype frequency.
Global 3.3%; European 2.5%; African 0.8%; East Asian 17.3%; South Asian 7.0%; Americas 7.4%; Ashkenazi 1.3%; Finnish 4.5%; Middle Eastern 0.8%; Amish 0.9%.
Estimated AA genotype frequency.
Showing effects for C/C genotype
Neurology & Mental Health
Addiction & Reward
Alcohol Use Disorder. Evidence: 4/10. Source: PMID 17196743. Typical Risk.
Opioid Addiction Risk. Evidence: 5/10. Source: PMID 24359476. Typical Risk.
Cocaine Addiction Risk. Evidence: 5/10. Source: PMID 21150907. Typical Risk.
Memory, Learning & Attention
Working Memory. Evidence: 5/10. Source: PMID 18077373. Typical Processing.
Pharmacogenomics
Antidepressant & Psychiatric Drug Response
Antipsychotic Response. Evidence: 5/10. Source: PMID 25563748. Typical Response.
Showing effects for A/A genotype
Alcohol Use Disorder. Evidence: 4/10. Source: PMID 17196743. ~1.3x Increased Risk.
Opioid Addiction Risk. Evidence: 5/10. Source: PMID 24359476. Increased Risk.
Cocaine Addiction Risk. Evidence: 5/10. Source: PMID 21150907. Increased Risk.
Working Memory. Evidence: 5/10. Source: PMID 18077373. Altered Processing.
Antipsychotic Response. Evidence: 5/10. Source: PMID 25563748. Stronger Response.
Showing effects for C/A genotype
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Balanced expression of the short presynaptic D2S receptor isoform relative to the long postsynaptic D2L isoform characterizes the C/C genotype [1]. This balanced ratio supports standard regulation of dopamine release in fronto-striatal brain circuits [1]. Research indicates that this genotype is associated with a baseline risk for alcohol, opioid, and cocaine dependence compared to carriers of the A allele [2]. In cognitive tasks, C/C carriers demonstrate typical working memory performance and standard neural activity patterns [1]. Additionally, some studies suggest a better response to certain medications like rasagiline, though response to other antipsychotics may be standard [3].
Typical dopamine receptor splicing; Baseline risk for substance dependence; Standard working memory processing.
Sample genotype: AA (Homozygous)
The lowest relative expression of the short presynaptic D2S receptor isoform occurs in those with the A/A genotype [1]. This significant reduction in D2S autoreceptors impairs the brain's ability to regulate synaptic dopamine levels, altering fronto-striatal signaling [1]. Consequently, this genotype is associated with an increased susceptibility to alcohol, opioid, and cocaine dependence [2]. In cognitive tasks, A/A carriers often show altered working memory processing, which may require greater neural activation to achieve similar performance levels [1]. Some studies also note differences in impulsivity and decision-making styles in those with this genetic profile [3]. However, this altered receptor profile is also linked to a potentially better response to antipsychotic treatments like olanzapine [4].
Reduced presynaptic D2S autoreceptor expression; Increased risk of substance dependence; Altered working memory and cognitive processing.
Sample genotype: CA (Heterozygous)
A reduced ratio of the short presynaptic D2S receptor isoform to the long postsynaptic D2L isoform is characteristic of the C/A genotype [1]. This shift alters the brain's natural feedback loop for dopamine release, particularly in regions governing reward and cognitive control [1]. Clinical studies have linked this genotype to an estimated 1.3-fold increased risk for alcohol dependence [2]. Research also indicates an elevated susceptibility to opioid and cocaine use disorders among carriers of this variant [3]. On the cognitive side, this altered dopaminergic tone can influence working memory processing and attentional control [1]. Interestingly, some pharmacogenomic studies suggest that C/A carriers may experience a better therapeutic response to certain antipsychotic medications like olanzapine [4].
Altered dopamine receptor isoform ratio; Slightly increased risk of alcohol and opioid dependence; Potential for better response to olanzapine.
Variants with shared genetic architecture
rs2514218 · DRD2 Gene · Chr 11 · Mental Health Risk
rs1801028 · DRD2 Gene · Chr 11 · Schizophrenia Risk
rs6277 · DRD2 Gene · Chr 11 · Dopamine Receptor Function
The dopamine receptor D2 (DRD2) SNP rs1076560 is associated with opioid addiction.
Genetic contributions to avoidance-based decisions: striatal D2 receptor polymorphisms.
Association analysis of the dopamine receptor D2 (DRD2) SNP rs1076560 in alcoholic patients.
Content updated August 2026.
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