LRRK2 and GBA in Parkinson’s Disease: What a Positive Genetic Result Really Means

LRRK2 and GBA in Parkinson’s Disease: What a Positive Genetic Result Really Means

This article is for educational purposes only. It is not a substitute for advice from a licensed physician, board-certified medical geneticist, or board-certified genetic counselor. For any decisions about testing, treatment, or care, consult a qualified clinician. In emergencies, call 911.

Bottom line: A large kin-cohort study estimated that only about 26 out of 100 people who carry the LRRK2 G2019S variant develop Parkinson’s disease by age 80. In plain terms, most carriers never develop it. GBA variants raise risk too, but research shows they act as a susceptibility factor, not a verdict. Knowing your variant is mainly an entry ticket to monitoring and research, not a diagnosis.

What you’ll learn:

• Why “dominant” does not mean “inevitable,” and how LRRK2 and GBA differ
• Your real, numeric lifetime risk — translated into “X out of 100 people”
• How a 23andMe result differs from a confirmatory clinical test
• What you can actually do now: monitoring, exercise, counseling, and research

LRRK2 and GBA: Two Very Different Genes

Your body carries two copies of most genes, one from each parent. LRRK2 (also called PARK8, on chromosome 12) and GBA (on chromosome 1) are the two most common genetic contributors to Parkinson’s disease. But they work in very different ways.

The most common Parkinson’s-linked LRRK2 change is called G2019S. It follows an autosomal-dominant pattern, meaning one copy of the variant, from either parent, is enough to raise risk. Yet “dominant” here does not mean “certain.” The variant has reduced, age-dependent penetrance, so a single copy elevates risk without guaranteeing disease. Penetrance simply means the share of carriers who actually develop the condition, and for G2019S that share is far below 100%.

GBA behaves differently. It is a susceptibility gene: a single variant meaningfully raises Parkinson’s risk without following the classic dominant or recessive pattern of certainty. National genetics references describe GBA as the most common genetic risk factor for Parkinson’s. One reason is that damaged versions of the gene impair how cells recycle waste. That can let a protein called alpha-synuclein build up, which is a hallmark of the disease.

GBA also has a second identity. The gene normally makes a lysosomal enzyme called glucocerebrosidase, and two damaged copies cause a separate condition called Gaucher disease, while one copy is a Parkinson’s risk factor. So a GBA result can carry meaning for both Parkinson’s risk and family planning, which is one more reason to review it with a professional.

At a glance, the two genes differ in a few key ways:

Feature	LRRK2 (G2019S)	GBA
Inheritance pattern	Autosomal-dominant, one copy raises risk	Susceptibility factor, not classic dominant/recessive
Penetrance	Reduced and age-dependent, far below 100%	Most single-copy carriers never develop PD
Second condition	None	Two copies cause Gaucher disease
Consumer test coverage	G2019S flagged	Only a short list of variants flagged

Think of it like weather risk. A dominant variant is not a guaranteed storm; it is a forecast that raises the odds. Your 23andMe report flags G2019S and a short list of GBA variants, but it does not read the whole gene. So a consumer result is a starting clue, not the full picture, as the testing section below explains.

If your report flagged either gene, a board-certified genetic counselor can explain exactly what your specific variant means. You can find one through the National Society of Genetic Counselors at NSGC.org.

Section recap: LRRK2 G2019S is dominant but incompletely penetrant. GBA is a susceptibility gene. Neither is a diagnosis, and consumer tests read only a few variants.

Why These Variants Cluster in Certain Families

Many readers first notice these variants because they seem to run in one branch of the family. There is a clear reason. Both LRRK2 G2019S and GBA variants are enriched in people of Ashkenazi Jewish descent.

The founder-population numbers make the clustering concrete:

• LRRK2 G2019S appears in roughly 10-15% of Ashkenazi Jewish Parkinson’s patients and about 1-2% of unaffected Ashkenazi individuals.
• LRRK2 in North Africa is also common in Berber and Arab populations, where it can account for up to 30-40% of Parkinson’s cases in some studies.
• GBA mutations were found in about 15% of Ashkenazi Jewish Parkinson’s patients versus about 3% of Ashkenazi controls in a large multicenter analysis.
• GBA carrier frequency among Ashkenazi Jews runs on the order of 1 in 12 to 1 in 16 people.

This is founder-population history, not ethnic destiny. Certain variants became common in a group long ago and were passed down, which is exactly why direct-to-consumer tests are built to surface them. Government references note that the single most common GBA variant among Ashkenazi Jews is called N370S, which accounts for a large share of the mutant copies in that population. That is one reason a consumer test can reliably screen for it.

It is worth keeping this clustering in perspective. Family enrichment explains why a variant appears, but it does not change the fact that most carriers, in any population, never develop Parkinson’s. A genetic counselor can help you read this family clustering without turning it into fear. You can start at NSGC.org.

Section recap: LRRK2 and GBA variants are common in Ashkenazi Jewish and, for LRRK2, North African founder populations. That explains family clustering without implying certainty.

Your Real Risk, Translated Into Numbers

The core fear is simple: does carrying this variant mean I will get Parkinson’s? Research says probably not. Here are the numbers, in plain form.

In the general population, the lifetime risk of Parkinson’s disease is roughly 1-2 out of 100 people. For LRRK2 G2019S carriers, a kin-cohort study of Ashkenazi Jewish families estimated the risk to age 80 at about 0.26. That is roughly 26 out of 100 carriers, meaning about 74 out of 100 never develop the disease. In that study, carriers had nearly a 3-fold higher risk than non-carriers, but the absolute number stayed well under half.

The absolute-risk estimates are easier to compare side by side:

Group / estimate	Reported risk	Source
General population, lifetime	~1-2 out of 100	baseline
LRRK2 G2019S, kin-cohort, to age 80	~26% (about 26 in 100)
LRRK2 G2019S, male carriers, to age 80	~22%
LRRK2 G2019S, female carriers, to age 80	~29%
LRRK2 G2019S, international case-control	~51% at age 69, ~74% at age 79
LRRK2 G2019S, summarized range	~25-75% by age and cohort

Estimates do vary by study. An earlier international case-control analysis, drawn from centers around the world, put cumulative G2019S risk higher, near 51% at age 69 and 74% at age 79. Curated clinical references summarize the range as roughly 25-75%, depending on age and cohort. Why such a spread? Different studies use different populations, ages, and methods, so no single figure is “the” answer. Even at the high end, this is a probability, not a certainty.

There is a reassuring detail in the sex breakdown too. In the kin-cohort study, penetrance was similar for men and women, roughly 22% for predicted male carriers and 29% for predicted female carriers to age 80. So this is not a risk that lands overwhelmingly on one sex.

GBA risk is severity-graded, meaning the specific variant matters. The strength of the association depends heavily on which variant you carry:

• Any GBA mutation: odds ratio about 5.4 in a large multicenter study of thousands of patients and controls.
• Mild variants: roughly a 2-to-5-fold increase in risk.
• Severe variants: can reach about 10-to-15-fold.
• Lower-risk variants: add only about 1.5-to-2-fold.
• Despite those multipliers, most single-copy GBA carriers never develop Parkinson’s.

That same multicenter study also found GBA-related Parkinson’s tended toward earlier onset and more cognitive involvement. An odds ratio can sound frightening, so it helps to translate it. Even a 5-fold jump on a baseline risk of about 1-2% still leaves the great majority of carriers unaffected. The multiplier is real, but it multiplies a small starting number, not a large one.

It also helps to zoom out. The largest genome study of Parkinson’s analyzed tens of thousands of patients and more than a million controls. It found 90 risk signals that together explain only about 16-36% of heritable risk. So any one flagged variant sits inside a much broader, partly non-genetic landscape. In plain terms, your genes are one input among many, not the whole story.

There is a reason researchers stress incomplete penetrance so heavily. When most carriers stay healthy, it means other factors, both genetic and environmental, help decide who develops disease. Those extra factors are still being mapped, which is another reason a gene result cannot predict your future with precision. A genetic counselor can turn these population numbers into a picture that fits your own history; start at NSGC.org.

Section recap: LRRK2 G2019S lifetime risk is commonly estimated near 26% and up to about 75% in some cohorts. GBA risk is severity-graded. Yet most carriers never develop Parkinson’s.

Testing: Consumer Kit Versus Clinical Test

A 23andMe report and a clinical genetic test are not the same thing. Consumer tests like 23andMe check only a few variants, reporting LRRK2 G2019S and a selected set of GBA variants. AncestryDNA does not report these clinical variants at all. So a consumer test can flag a variant, but it is a screen, not a final answer.

The three main testing routes differ in what they cover, who orders them, and what they cost:

Testing route	What it reads	Who orders / cost	Best for
Consumer kit (23andMe)	G2019S + a short GBA list only	Self-ordered, consumer-priced	A first screen, not confirmation
Clinical lab (Invitae, Color)	Broad, physician-ordered panels	Physician-ordered	Confirming a consumer positive
PD GENEration	Major PD genes incl. LRRK2 + GBA	Free, for diagnosed patients; counselor review; ~2 months	Diagnosed patients wanting counseled, no-cost testing

Two limits matter. First, a positive consumer result should be confirmed with a clinical-grade test before you treat it as fact. Second, a negative consumer result does not rule out other risk variants, because the panel reads only a short list. In other words, “not detected” is not the same as “not present.”

For confirmation, clinical laboratories such as Invitae or Color offer physician-ordered genetic testing. There is also a strong no-cost option for people already diagnosed with Parkinson’s. The Parkinson’s Foundation runs a research program called PD GENEration that offers free, clinical-grade genetic testing plus certified genetic-counselor results review. Its panel covers major Parkinson’s genes, including LRRK2 and GBA, and results return in about two months.

Why confirm at all? A clinical-grade test is run and interpreted under stricter standards, and it usually comes with counseling built in. That matters, because how a result is explained shapes how a person copes with it. PD GENEration, for example, returns results with a certified genetic counselor’s review rather than as a raw data point.

Think of the consumer kit as a smoke detector and the clinical test as the fire inspector. The detector is worth having, but you confirm before you act. A genetic counselor can help you choose the right confirmatory path. You can find one at NSGC.org.

Section recap: Consumer kits screen only a few variants and should be confirmed clinically. PD GENEration offers free, counseled testing for diagnosed patients.

What a Positive Result Does and Does Not Mean

A positive LRRK2 or GBA result is a risk finding, not a Parkinson’s diagnosis. Parkinson’s is still diagnosed clinically, by a doctor examining movement for signs like slowness (bradykinesia), stiffness, and tremor, sometimes supported by imaging. A gene result cannot make that diagnosis on its own.

It also helps to know that G2019S-related Parkinson’s, when it does occur, looks much like ordinary Parkinson’s on exam. That is why the clinical picture, not the gene alone, drives diagnosis.

Research is opening a new window, though. In 2023, a large study applied an alpha-synuclein seed amplification assay (a lab test that detects a misfolded brain protein linked to Parkinson’s) to more than 1,100 study participants. It was about 93% sensitive in typical Parkinson’s and even detected the protein in some at-risk people before symptoms appeared. Interestingly, sensitivity was lower in LRRK2 carriers, near 68%, showing not all genetic Parkinson’s shows the same biology.

This test is exciting, but it is a research and emerging tool, not something you can simply order at a clinic. It is best understood as a window researchers are still learning to use, not a diagnosis you can request today. That is an important distinction, because headlines about “detecting Parkinson’s early” can imply the test is widely available when it is not.

One more caution: many gene variants are of uncertain significance, meaning experts do not yet know if they raise risk. These should not be over-interpreted, and a counselor can tell you which category your result falls into. The identity of the specific variant matters here. As one study of GBA variants showed, “GBA positive” is not a single risk level; a mild variant and a severe variant carry very different odds. You can start at NSGC.org.

Section recap: A gene result is a risk flag, not a diagnosis. The 2023 alpha-synuclein assay is a promising research tool, not a routine clinical order.

Prevention, Surveillance, and Early Detection

There is no proven way to prevent Parkinson’s disease. That is the honest starting point. But it does not mean there is nothing constructive to do.

One evidence-linked step is exercise. Prospective and pooled studies found that higher physical activity is associated with lower Parkinson’s risk, with a pooled hazard ratio near 0.66. That is roughly a one-third lower risk in the most active groups. This is an observed association, not proof that exercise stops Parkinson’s in a gene carrier, so it is a reasonable step, not a guarantee.

Monitoring matters too. Certain early, “prodromal” signs can appear years before movement problems. In a known carrier, these are worth mentioning to a specialist rather than dismissing:

• REM sleep behavior disorder — acting out dreams during sleep.
• Hyposmia — a reduced sense of smell.
• Constipation — a persistent change in bowel habits.

If these appear, a neurologist or movement-disorder specialist is the right person to see. They can track subtle changes over time.

None of these signs, on their own, means Parkinson’s is coming. Each is common for other reasons too. But in a known carrier, they are worth mentioning to a specialist rather than dismissing. The value is in careful follow-up, not self-diagnosis.

Another constructive option is joining a long-term research cohort. One example is the Parkinson’s Progression Markers Initiative, which followed more than a thousand participants, including at-risk people, over time. Enrolling does two useful things. It gives you structured, expert follow-up, and it contributes data that may help clarify the very penetrance questions that worry carriers.

Be cautious about supplements marketed to “prevent” Parkinson’s; the evidence does not support overselling them. Exercise, by contrast, has genuine observational support and broad general-health benefits, which makes it a low-risk step worth taking regardless. Your primary care provider or a genetic counselor can help you build a monitoring plan. You can find a counselor at NSGC.org.

Section recap: No proven prevention exists, but exercise is linked to lower risk. Monitoring for early signs plus research-cohort enrollment are reasonable, evidence-based steps.

The Treatment Landscape and Where the Drugs Stand

Standard treatment for Parkinson’s remains symptom control, mainly levodopa-based therapy. Levodopa and carbidopa are long approved by the FDA, but they treat symptoms only; they do not slow the disease and are not gene-targeted. There is no cure.

The genetically exciting frontier is disease-modifying drugs aimed at LRRK2 and GBA. It is important to be clear and current about their status. As of 2026, no LRRK2- or GBA-targeted disease-modifying drug is approved by the FDA or Health Canada. The table below summarizes where each stands:

Drug / therapy	Target	Regulatory status (2026)
Levodopa + carbidopa	Symptom control, not gene-targeted	FDA-approved; treats symptoms only, does not slow disease
BIIB122 / DNL151	LRRK2 kinase inhibitor	Investigational; idiopathic-PD development discontinued, carrier-only Phase 2a BEACON active
Ambroxol	Raises glucocerebrosidase (GBA)	Investigational; not FDA/Health Canada-approved as disease-modifying

For LRRK2, the leading candidate was an oral kinase inhibitor called BIIB122 (also DNL151), from Biogen and Denali. In early testing it strongly blocked LRRK2 activity, cutting the enzyme’s measured activity by more than 90%. That kind of target engagement is what researchers hope to see. But biological effect is not the same as clinical benefit.

Here the story turned. Its Phase 2b LUMA study in early Parkinson’s reported topline results in 2026. On that basis, the companies discontinued development in idiopathic, meaning non-inherited, Parkinson’s, and the Phase 3 LIGHTHOUSE study was terminated. Reports cited program complexity and timelines rather than a new safety alarm. Only the Phase 2a BEACON study, specifically for people who carry a pathogenic LRRK2 variant, remained active. This is the honest headline: for a variant carrier, genetic status confers trial eligibility, not a treatment. It is why a positive result can open a research door, but not a pharmacy one.

For GBA, the picture is early. A small open-label trial of a repurposed drug called ambroxol enrolled 17 patients, with and without GBA variants. It found the drug was safe, reached the brain, and raised the target enzyme, glucocerebrosidase. But it was not a controlled efficacy trial and did not prove clinical benefit. Ambroxol remains investigational for Parkinson’s and is not FDA- or Health Canada-approved as a disease-modifying therapy; larger controlled trials are ongoing.

The honest summary across both genes is the same. The science is genuinely promising, but promise is not approval. That distinction protects you from paying for or pinning hope on a therapy that has not yet shown it changes the course of disease. If trial participation interests you, discuss eligibility with a neurologist or genetic counselor. You can start at NSGC.org.

Section recap: Levodopa treats symptoms only. As of 2026 no LRRK2- or GBA-targeted disease-modifying drug is approved. Genetic status affects trial eligibility, not treatment.

Family Implications and Cascade Testing

Because LRRK2 G2019S is dominant, first-degree relatives have their own inheritance odds. Each child and sibling of a carrier has about a 50% chance of inheriting the variant. But this bears repeating: inheriting the variant is not inheriting the disease, because penetrance is incomplete. If lifetime risk in carriers is roughly one in four, then a relative who inherits the variant still, more likely than not, never develops Parkinson’s.

For a parent, this reframes a painful worry. Passing on a variant is not the same as passing on a fate. It passes on a raised probability that, for most, never becomes disease.

GBA inheritance is more layered. It acts as a susceptibility factor for Parkinson’s, and it carries a second consideration: two GBA variants together cause Gaucher disease, which matters for reproductive planning. So a GBA finding can touch both Parkinson’s risk and family-planning questions. Take a couple who each carry a GBA variant. A counselor can explain their separate, small chance of Gaucher disease in a child. That is a different question from adult Parkinson’s risk, and it deserves its own conversation.

The organized way to explore this in a family is cascade testing, meaning testing relatives step by step after one person tests positive. But it is not a do-it-yourself project. Predictive or cascade testing, especially of children, should be paired with genetic counseling first. Testing a child without counseling can create anxiety over a risk that may never materialize, and the child cannot yet give informed consent for a predictive result.

Think of cascade testing like sharing important but sensitive family news: how and when you do it matters. A board-certified genetic counselor, found through the National Society of Genetic Counselors or the American Board of Genetic Counseling, can guide the process. You can start at NSGC.org.

Section recap: First-degree relatives have about a 50% chance of inheriting LRRK2 G2019S, but not the disease. Cascade testing, especially of children, should follow genetic counseling.

Psychosocial Impact, Insurance, and Disclosure

A positive predictive result carries emotional weight, even when the numbers are reassuring. That is normal, and it is a reason to pair testing with counseling rather than facing it alone.

It is worth naming the feeling directly. Many carriers describe a quiet dread of being “next,” or guilt about what they may have passed to their children. Neither feeling is unreasonable, and neither is a reliable guide to the actual odds. This is exactly where a counselor helps: translating a scary label into a grounded, numeric picture you can live with.

Insurance protection differs sharply between the two countries. The contrast is worth seeing side by side:

Protection	United States (GINA, 2008)	Canada (GNDA, 2017)
Health insurance	Protected	Protected
Employment	Protected	Protected
Life insurance	Not covered	Covered
Disability insurance	Not covered	Covered
Long-term-care insurance	Not covered	Covered
Legal force	Federal statute; some states add more	Criminal offense to require genetic results; upheld by Supreme Court of Canada, July 10, 2020

In the US, the Genetic Information Nondiscrimination Act of 2008 (GINA) prohibits genetic discrimination in health insurance and in employment. That is real protection. But GINA has a real gap: it does not cover life insurance, disability insurance, or long-term-care insurance. For a Parkinson’s-risk finding, that gap is worth knowing before you buy such policies, and some US states add further protection.

Canada is different. Its Genetic Non-Discrimination Act of 2017 is broader. It makes it a criminal offense to require or use genetic test results as a condition of providing goods or services, including insurance. The Supreme Court of Canada upheld this law as constitutional on July 10, 2020. So Canadian readers generally have wider coverage than US readers.

A practical takeaway follows from this. If you live in the US and are weighing life, disability, or long-term-care insurance, it can be worth understanding your options before testing, since that is where the federal law leaves a gap. This is not a reason to avoid testing. It is a reason to make the decision with clear information, ideally alongside a counselor.

Deciding whether to tell siblings or children is personal, and there is no single right script. Some relatives want to know so they can plan or join research. Others would rather not carry a probability they cannot change. Both choices are valid. It is best made as a counseled decision, weighing what relatives may want to know against the emotional cost. A genetic counselor can help you think it through without pressure, and can help you find the words. You can find one at NSGC.org.

Section recap: GINA protects US health insurance and employment but not life, disability, or long-term-care coverage. Canada’s 2017 law is broader. Disclosure to family is a personal, counseled choice.

Frequently Asked Questions

Q1. If I carry the LRRK2 G2019S variant, will I get Parkinson’s disease?

Probably not. A kin-cohort study estimated lifetime risk to age 80 at about 26%, so roughly 74 out of 100 carriers never develop it. Other cohorts estimate higher, up to about 75%, but every estimate is a probability, not a certainty. Reduced penetrance means other genes and environment also shape the outcome.

Q2. Will my children inherit Parkinson’s from me?

Not necessarily. Because LRRK2 G2019S is dominant, each child has about a 50% chance of inheriting the variant. But inheriting the variant is not inheriting the disease, given incomplete penetrance. Discuss cascade testing with a genetic counselor before testing relatives, especially children.

Q3. Will this genetic result affect my health or life insurance?

In the US, GINA protects health insurance and employment, but it does not cover life, disability, or long-term-care insurance. That last gap is real for a Parkinson’s-risk finding. In Canada, the 2017 law is broader and covers insurance contracts more fully.

Q4. Can my employer find out about my result?

In the US, GINA prohibits genetic discrimination in employment. In Canada, the Genetic Non-Discrimination Act makes it a criminal offense to require genetic results as a condition of services. A genetic counselor can explain how these protections apply to your situation; start at NSGC.org.

Q5. Should I confirm my 23andMe result with a real test?

Yes. Consumer tests read only a few variants, so a positive result should be confirmed clinically, through labs like Invitae or Color or through PD GENEration. A negative consumer result also does not rule out other variants, because the panel is limited.

The Takeaway

Research shows that a LRRK2 or GBA variant raises Parkinson’s risk without making it certain. A kin-cohort study put LRRK2 G2019S lifetime risk near 26%, and multicenter research frames GBA as a susceptibility factor most carriers never act on. “Higher than average” is not “inevitable.”

This same research also points to constructive steps. Confirm a consumer result with a clinical or research-grade test. Watch for early signs and stay active, since exercise is linked to lower risk. Consider a research cohort, where knowing your gene status can open doors.

Be clear-eyed about treatment. As of 2026, no LRRK2- or GBA-targeted disease-modifying drug is FDA- or Health Canada-approved. The leading LRRK2 program stopped its idiopathic-Parkinson’s work while continuing a carrier-only trial. For now, genetic status is an entry ticket to research and monitoring, not a prescription.

You do not have to sort any of this out alone. A board-certified genetic counselor is a reliable starting point, and you can search for one at NSGC.org. Your primary care provider or a neurologist is another. They can turn these population numbers into a plan that fits your own family history.

This article is for educational purposes only. It is not a substitute for advice from a licensed physician, board-certified medical geneticist, or board-certified genetic counselor. For any decisions about testing, treatment, or care, consult a qualified clinician. In emergencies, call 911 (US/Canada) or 119 (Japan).

References

1. Marder K, Wang Y, Alcalay RN, et al. (2015) Age-specific penetrance of LRRK2 G2019S in the Michael J. Fox Ashkenazi Jewish LRRK2 Consortium. Neurology. https://pmc.ncbi.nlm.nih.gov/articles/PMC4501942/
2. Healy DG, Falchi M, O’Sullivan SS, et al. (2008) Phenotype, genotype, and worldwide genetic penetrance of LRRK2-associated Parkinson’s disease. Lancet Neurology. https://pmc.ncbi.nlm.nih.gov/articles/PMC2832754/
3. Sidransky E, Nalls MA, Aasly JO, et al. (2009) Multicenter Analysis of Glucocerebrosidase Mutations in Parkinson’s Disease. New England Journal of Medicine. https://pmc.ncbi.nlm.nih.gov/articles/PMC2856322/
4. Gan-Or Z, Amshalom I, Kilarski LL, et al. (2015) Differential effects of severe vs mild GBA mutations on Parkinson disease. Neurology. https://pmc.ncbi.nlm.nih.gov/articles/PMC4351661/
5. Siderowf A, Concha-Marambio L, Lafontant DE, et al. (2023) Assessment of heterogeneity among PPMI participants using alpha-synuclein seed amplification. Lancet Neurology. https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(23)00109-6/abstract
6. Nalls MA, Blauwendraat C, Vallerga CL, et al. (2019) Identification of novel risk loci, causal insights, and heritable risk for Parkinson’s disease. Lancet Neurology. https://pubmed.ncbi.nlm.nih.gov/31701892/
7. Mullin S, Smith L, Lee K, et al. (2020) Ambroxol for the Treatment of Patients With Parkinson Disease With and Without Glucocerebrosidase Gene Mutations (AiM-PD). JAMA Neurology. https://pmc.ncbi.nlm.nih.gov/articles/PMC6990847/
8. Biogen & Denali Therapeutics (2024-2026). LRRK2 kinase inhibitor BIIB122 / DNL151 clinical development update (LUMA, LIGHTHOUSE, BEACON). https://investors.biogen.com/news-releases/news-release-details/biogen-and-denali-therapeutics-provide-update-phase-2b-luma
9. National Institute of Neurological Disorders and Stroke (NINDS/NIH). Parkinson’s Disease — Health Information (including Genetics: LRRK2 and GBA1). https://www.ninds.nih.gov/health-information/disorders/parkinsons-disease
10. MedlinePlus Genetics (NIH/NLM). GBA1 gene. https://medlineplus.gov/genetics/gene/gba1/
11. Cook Shukla L, Schulze J, Farlow J, et al. GeneReviews (NIH/NCBI Bookshelf). LRRK2-Related Parkinson Disease. https://www.ncbi.nlm.nih.gov/books/NBK1208/
12. Parkinson’s Foundation. PD GENEration: Mapping the Future of Parkinson’s Disease (free genetic testing + counseling). https://www.parkinson.org/advancing-research/our-research/pdgeneration
13. National Human Genome Research Institute (NHGRI/NIH); Supreme Court of Canada (2020). Genetic Discrimination: GINA (US, 2008) and Canada’s Genetic Non-Discrimination Act (2017). https://www.genome.gov/about-genomics/policy-issues/Genetic-Discrimination
14. Yang F, Trolle Lagerros Y, Bellocco R, et al. (2015) Physical activity and risk of Parkinson’s disease (Swedish National March Cohort) and pooled prospective analyses. Brain. https://pubmed.ncbi.nlm.nih.gov/25516395/

Last updated: 2026-07-12

Author: Yu Mizuno (Editor-in-Chief, non-physician), GeneLumen editorial team. This article aggregates 14 sources from peer-reviewed medical literature and public health agencies (tier 1=A / tier 2=B). Sources include NIH/NINDS, MedlinePlus, GeneReviews, FDA/Health Canada regulatory status, and PubMed-indexed publications. Sources are tier-rated: tier 1=12, tier 2=2.

This article is for educational purposes only and is not a substitute for medical advice from a licensed physician, board-certified medical geneticist, or board-certified genetic counselor. In emergencies, call 911 (US/Canada) or 119 (Japan).

Related: Genetic Diseases category

🇯🇵 For readers in Japan — a separate Japanese edition written for Japan’s healthcare system (not a translation): https://genelumen.com/ja/ja-neurogenetic/lrrk2-gba-parkinsons-disease-genetic-risk