What you carry at this position in your DNA and what research says about it.
Parkinson Disease Risk: 10/10 evidence, 22 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): G/G
Typical Parkinson Disease Risk
Two copies of the common G allele indicate a standard baseline risk for Parkinson's disease. No elevated genetic risk for LRRK2-related inflammatory or oncological conditions is present.
What this genotype means: Typical baseline risk for Parkinson's disease; Normal LRRK2 kinase enzyme activity.
Sample genotype (not yours): A/A
Significantly Higher Parkinson Disease Risk
Two copies of the A allele significantly increase the lifetime risk of developing Parkinson's disease, with clinical outcomes similar to carrying a single copy. It is also associated with elevated risks of Crohn's disease and certain cancers.
What this genotype means: Significantly elevated risk of Parkinson's disease; Increased risk of Crohn's disease; Slightly increased risk of colon cancer and leukemia.
Sample genotype (not yours): G/A
One copy of the A allele significantly increases the lifetime risk of developing Parkinson's disease, though many carriers never develop it. It is also linked to moderately higher risks of Crohn's disease and certain cancers.
Gene function and biological role
Gene Function: The LRRK2 gene encodes a large, multi-domain enzyme called leucine-rich repeat kinase 2, which plays a critical role in cellular waste clearance and immune responses [1]. This kinase is highly active in immune cells and brain tissues, where it regulates the function of other proteins involved in vesicle trafficking and lysosomal degradation [1]. When LRRK2 function is altered, it can lead to the accumulation of toxic protein aggregates, particularly alpha-synuclein, which is a hallmark of neurodegenerative processes [2]. Beyond the brain, LRRK2 is also active in the gut, where it modulates inflammatory pathways and intestinal barrier integrity [3].
Variant Impact: The rs34637584 variant, widely known as the G2019S mutation, is a missense change that alters a single amino acid from glycine to serine at position 2019 of the LRRK2 protein [4]. This specific alteration occurs in the highly conserved kinase domain of the enzyme, causing it to become constitutively hyperactive [1]. The resulting overactivity triggers excessive phosphorylation of downstream target proteins, disrupting vital cellular transport and waste disposal systems [5]. This molecular dysfunction is a major genetic driver of both familial and sporadic forms of Parkinson's disease [2].
Key Insight: Although this variant is one of the strongest genetic risk factors for Parkinson's disease, it has incomplete penetrance, meaning many people who carry it live a full life without ever developing the condition.
Location: LRRK2. Chromosome 12 · 12q12 · 40.3 Mb
Origin Story: The G2019S mutation on the main haplotype is believed to have originated in a common ancestor in the Middle East or North Africa several thousand years ago, later spreading through founder effects in Ashkenazi Jewish and Arab-Berber populations.
Estimated prevalence by population
Global 99.9%; European > 99.9%; African 100.0%; East Asian 100.0%; South Asian 100.0%; Americas 99.8%; Ashkenazi 98.9%; Middle Eastern 99.3%; Amish 100.0%.
Estimated GG genotype frequency.
Global 0.1%; European < 0.1%; African 0.0%; East Asian 0.0%; South Asian 0.0%; Americas 0.2%; Ashkenazi 1.1%; Middle Eastern 0.7%; Amish 0.0%.
Estimated GA genotype frequency.
Global < 0.1%; European < 0.1%; African 0.0%; East Asian 0.0%; South Asian 0.0%; Americas < 0.1%; Ashkenazi < 0.1%; Middle Eastern < 0.1%; Amish 0.0%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Neurology & Mental Health
Neurodegenerative Diseases
Parkinson's Disease. Evidence: 10/10. Source: PMID 21738487. Typical.
Immunity & Inflammation
Chronic Inflammatory Diseases
Crohn's Disease. Evidence: 4/10. Source: PMID 21812969. Typical.
Cancer & Oncology
Colorectal Cancer
Colorectal Cancer. Evidence: 3/10. Source: PMID 20197411. Typical.
Blood Cancers
Leukemia. Evidence: 3/10. Source: PMID 20197411. Typical.
Showing effects for A/A genotype
Parkinson's Disease. Evidence: 10/10. Source: PMID 21738487. 9.6x Higher Risk.
Crohn's Disease. Evidence: 4/10. Source: PMID 21812969. Increased Risk.
Colorectal Cancer. Evidence: 3/10. Source: PMID 20197411. ~2x Higher Risk.
Leukemia. Evidence: 3/10. Source: PMID 20197411. ~10x Higher Risk.
Showing effects for G/A genotype
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Two copies of the standard G allele represent the typical genetic baseline for the general population. The absence of the G2019S mutation means the LRRK2 kinase enzyme functions at normal, regulated levels [1]. Consequently, there is no elevated risk for LRRK2-related neurodegeneration or associated lysosomal dysfunction [2]. Standard age-related risks for Parkinson's disease still apply, but they are not amplified by this specific genetic factor [3]. Similarly, risks for associated inflammatory conditions like Crohn's disease remain at the typical population baseline [4]. Maintaining healthy lifestyle habits, such as regular exercise and a balanced diet, remains the best approach for long-term brain health.
Typical baseline risk for Parkinson's disease; Normal LRRK2 kinase enzyme activity.
Sample genotype: AA (Homozygous)
Two copies of the rare A allele are extremely uncommon and result in a double dose of the hyperactive G2019S LRRK2 enzyme [1]. Clinical studies of individuals with two copies show that the risk and progression of Parkinson's disease are highly similar to those with only one copy [2]. The lifetime probability of developing Parkinson's remains significantly elevated, yet incomplete penetrance is still observed, with some homozygous individuals remaining symptom-free into older age [3]. This genotype also promotes systemic inflammation, raising the risk of Crohn's disease due to altered immune responses in the gut [4]. Furthermore, the hyperactive kinase activity is linked to an increased susceptibility to colon cancer and leukemia [5]. Close coordination with healthcare providers for neurological and systemic health screenings is highly recommended for individuals with this genetic profile.
Significantly elevated risk of Parkinson's disease; Increased risk of Crohn's disease; Slightly increased risk of colon cancer and leukemia.
Sample genotype: GA (Heterozygous)
Inheriting one copy of the A allele introduces the G2019S mutation, which causes LRRK2 kinase activity to become hyperactive [1]. This hyperactivity is a well-established genetic driver that raises the lifetime risk of Parkinson's disease to between 15% and 30%, and potentially higher at advanced ages [2]. However, the mutation has incomplete penetrance, meaning that a significant portion of carriers remain completely healthy throughout their lives [3]. The elevated kinase activity also impacts peripheral tissues, moderately increasing susceptibility to inflammatory bowel conditions like Crohn's disease [4]. Additionally, some evidence suggests carriers may face an increased risk of certain cancers, such as colon cancer and leukemia [5]. Regular clinical monitoring and proactive lifestyle strategies, such as physical exercise, can help manage overall neurological health.
Variants with shared genetic architecture
rs34778348 · LRRK2 Gene · Chr 12 · Parkinson Disease Risk
rs10411210 · RHPN2 Gene · Chr 19 · Colorectal Cancer Risk
rs10486567 · JAZF1 Gene · Chr 7 · Prostate Cancer Risk
A common LRRK2 mutation in idiopathic Parkinson's disease.
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