LRRK2 — Leucine Rich Repeat Kinase 2

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LRRK2 — Leucine Rich Repeat Kinase 2

<table class="infobox infobox-gene">
<tr>
<th class="infobox-header" colspan="2">LRRK2 — Leucine Rich Repeat Kinase 2</th>
</tr>
<tr>
<td class="label">Symbol</td>
<td><strong>LRRK2</strong></td>
</tr>
<tr>
<td class="label">Full Name</td>
<td>Leucine Rich Repeat Kinase 2</td>
</tr>
<tr>
<td class="label">Chromosome</td>
<td>12q12</td>
</tr>
<tr>
<td class="label">NCBI Gene</td>
<td><a href="https://www.ncbi.nlm.nih.gov/gene/120892" target="_blank">120892</a></td>
</tr>
<tr>
<td class="label">Ensembl</td>
<td><a href="https://ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000188906" target="_blank">ENSG00000188906</a></td>
</tr>
<tr>
<td class="label">OMIM</td>
<td><a href="https://omim.org/entry/609007" target="_blank">609007</a></td>
</tr>
<tr>
<td class="label">UniProt</td>
<td><a href="https://www.uniprot.org/uniprot/Q5S007" target="_blank">Q5S007</a></td>
</tr>
<tr>
<td class="label">Diseases</td>
<td>[Parkinson's Disease](/diseases/parkinsons-disease)</td>
</tr>
<tr>
<td class="label">Expression</td>
<td>Striatum, Cerebral cortex, Kidney, Lungs</td>
</tr>
<tr>
<th class="infobox-subheader" colspan="2">Key Mutations</th>
</tr>
<tr>
<td colspan="2" style="font-size:0.85em">G2019S, R1441C/G/H, Y1699C, I2020T</td>
</tr>
<tr>
<td class="label">Associated Diseases</td>
<td><a href="/wiki/als" style="color:#ef9a9a">ALS</a>, <a href="/wiki/alzheimer" style="color:#ef9a9a">ALZHEIMER</a>, <a href="/wiki

...

LRRK2 — Leucine Rich Repeat Kinase 2

Overview

Lrrk2 — Leucine Rich Repeat Kinase 2 plays an important role in the study of neurodegenerative diseases. This page provides comprehensive information about this topic, including its mechanisms, significance in disease processes, and therapeutic implications.

Introduction

LRRK2 (Leucine-Rich Repeat Kinase 2), also known as dardarin, is a large multi-domain protein kinase encoded by the LRRK2 gene on chromosome 12q12[@paisnruz2004]. It is one of the most common genetic causes of Parkinson's disease (PD), with pathogenic mutations accounting for approximately 5-10% of familial PD cases and 1-3% of sporadic PD cases[@cookson2023]. The LRRK2 protein is a member of the ROCO family of Ras-of-Complex (ROC) proteins and possesses both kinase and GTPase activity.

The discovery of LRRK2 mutations as a cause of PARK8-linked Parkinson's disease in 2004 marked a major breakthrough in understanding the genetics of PD and has led to extensive research into its function and therapeutic targeting[@zimprich2004][@alessi2018].

Structure

AlphaFold DB provides a full-length predicted structure for LRRK2 (UniProt [Q5S007](https://www.uniprot.org/uniprotkb/Q5S007/entry), model v6) with mean pLDDT 77.5. View the model at [AlphaFold DB](https://alphafold.ebi.ac.uk/entry/Q5S007) or download the [PDB file](https://alphafold.ebi.ac.uk/files/AF-Q5S007-F1-model_v6.pdb).

Domain and region confidence from per-residue pLDDT:

Residues 1-969 (Required for RAB29-mediated activation): mean pLDDT 72.6 (confident).
Residues 319-348 (Coiled coil): mean pLDDT 51.1 (low).
Residues 1328-1511 (Roc): mean pLDDT 78.7 (confident).
Residues 1546-1740 (COR): mean pLDDT 76.8 (confident).
Residues 1879-2138 (Protein kinase): mean pLDDT 80.3 (confident).
Residues 2139-2183 (WD 1): mean pLDDT 81.0 (confident).
Residues 2281-2327 (WD 4): mean pLDDT 83.8 (confident).
Residues 2443-2497 (WD 7): mean pLDDT 75.8 (confident).

Overall confidence distribution: 345 residues (14%) very high, 1659 residues (66%) confident, 302 residues (12%) low, 221 residues (9%) very low. Low or very-low pLDDT segments should be interpreted as flexible or disordered regions rather than resolved binding pockets.

UniProt function annotation: Serine/threonine-protein kinase which phosphorylates a broad range of proteins involved in multiple processes such as neuronal plasticity, innate immunity, autophagy, and vesicle trafficking (PubMed:17114044, PubMed:20949042, PubMed:21850687, PubMed:22012985, PubMed:23395371, PubMed:24687852, PubMed:25201882, PubMed:26014385, PubMed:26824392.
Subcellular localization: Cytoplasmic vesicle, Perikaryon, Golgi apparatus membrane, Cell projection, axon, Cell projection, dendrite, Endoplasmic reticulum membrane, Cytoplasmic vesicle, secretory vesicle, synaptic vesicle membrane, Endosome.
Curated disease associations include: Parkinson disease 8.

Normal Function

Under physiological conditions, LRRK2 participates in multiple cellular processes:

Cellular Signaling

LRRK2 acts as a molecular scaffold for various signaling pathways:

MAPK signaling: Modulates ERK, JNK, and p38 pathways
Wnt signaling: Interacts with β-catenin pathway components
mTOR signaling: Regulates autophagy and cell growth

Cytoskeletal Functions

Actin cytoskeleton: Regulates actin dynamics and cell morphology
Microtubule function: Associates with microtubules, affects transport
Neurite outgrowth: Promotes neuronal process extension

Membrane Trafficking

Endocytosis: Regulates vesicle trafficking and receptor internalization
Lysosomal function: Involved in autophagy-lysosome pathway
Synaptic transmission: Modulates synaptic vesicle release

Inflammation

Microglial activation: Regulates inflammatory responses
Cytokine production: Affects neuroinflammation in PD[@tolosa2022]

Tissue Expression

LRRK2 is widely expressed with highest levels in:

Brain: Striatum, cerebral cortex, hippocampus, cerebellum
Peripheral organs: Kidney, lungs, lymph nodes
Immune cells: Monocytes, macrophages, B-cells

Pathogenesis in Parkinson's Disease

Genetic Evidence

LRRK2 mutations are the most common known genetic cause of PD:

G2019S: Most common pathogenic mutation (~5% familial, ~1% sporadic)
Located in kinase domain activation loop
Increases kinase activity by 2-3 fold
Penetrance: ~70% by age 80
R1441C/G/H: Located in ROC domain
Reduces GTPase activity
Causes constitutive activation
Y1699C: Located in COR domain
Impairs dimerization
Increases kinase activity
I2020T: Located in kinase domain
Increases autophosphorylation

Mechanisms of Neurodegeneration

LRRK2 mutations cause neuronal dysfunction through several mechanisms:

Kinase hyperactivity: Enhanced phosphorylation of substrates

Dysregulated GTPase activity: Impaired ROC domain function

Mitochondrial dysfunction: Altered mitochondrial dynamics

Autophagy impairment: Defective lysosomal degradation

Synaptic dysfunction: Altered neurotransmitter release

Neuroinflammation: Microglial activation

Substrate Phosphorylation

Key LRRK2 substrates include:

Rab proteins (Rab3, Rab5, Rab7, Rab10, Rab12): Vesicle trafficking
MAP1B: Microtubule-associated protein
ERK1/2: Cell signaling
Tau: Microtubule stability
α-Synuclein: Aggregation modulation

Recent Research Updates (2025-2026)

Recent studies have advanced our understanding of LRRK2 function and its role in Parkinson's disease:

LRRK2-mediated pyroptosis: Research demonstrates that LRRK2 mediates pyroptosis via the NLRP3/Caspase-1/GSDMD pathway in Parkinson's disease progression[@paisnruz2004].

Therapeutic Targeting

LRRK2 represents one of the most promising therapeutic targets in PD drug development:

Kinase Inhibitors

Multiple LRRK2 inhibitors are in clinical development:

DNL151/DNL312: Denali Therapeutics - Phase 1/2 trials
BIIB122 (DNL151): Biogen partnership - Phase 1b
PF-06649751: Pfizer - Phase 1
GZ-161: Gains in preclinical models

These inhibitors aim to:

Reduce kinase activity to normal levels
Prevent neurodegeneration
Potentially reverse pathology

Challenges

Peripheral toxicity: Kidney and lung side effects
Blood-brain barrier penetration: Required for CNS effect
Biomarkers: Need for patient selection
Genetic complexity: Variable penetrance

Other Therapeutic Approaches

Antisense oligonucleotides: Gene silencing approaches
Protein-protein interaction inhibitors: Block pathogenic interactions
GTPase activators: Enhance ROC domain function

Gene Therapy Approaches

Gene therapy for LRRK2-associated neurodegeneration represents a promising frontier for disease modification. Unlike small molecule inhibitors that require chronic dosing and may have peripheral toxicity, gene therapy approaches aim to provide durable, potentially curative treatment by directly addressing the genetic basis of the disease.

Antisense Oligonucleotides (ASOs)

Antisense oligonucleotides are single-stranded DNA sequences that bind to complementary mRNA, preventing translation or promoting degradation:

Mechanism: ASOs bind to LRRK2 mRNA, reducing protein translation through RNase H-mediated cleavage
Advantages: Sequence-specific targeting, can reduce LRRK2 expression without affecting other kinases
Challenges: Blood-brain barrier penetration, delivery to target neurons, dosing frequency
Current status: Preclinical development, with promising results in mouse models showing reduced LRRK2 expression and improved phenotypes
Delivery methods: Intrathecal injection, convection-enhanced delivery

RNA Interference (RNAi)

RNAi uses small interfering RNAs (siRNAs) or short hairpin RNAs (shRNAs) to silence gene expression:

Viral-delivered shRNA: AAV vectors carrying shRNA cassettes targeting LRRK2
Target regions: 5' UTR and coding sequences to maximize knockdown
Efficacy: Up to 80% reduction of LRRK2 expression in preclinical models
Considerations: Off-target effects, immune response to viral delivery

CRISPR-Based Gene Editing

Gene editing technologies offer the potential to directly correct pathogenic mutations:

Base editing: Precise single-nucleotide changes without double-strand breaks
Prime editing: Insertions, deletions, and replacements
AAV-delivered Cas9: System for in vivo editing of neurons
Challenges: Efficiency of editing in post-mitotic neurons, delivery to specific brain regions
Future potential: Mutation-specific correction for patients with LRRK2 kinase-activating mutations

Viral Vector Delivery Systems

| Vector | Tropism | Capacity | Duration | Clinical Status |
|--------|---------|----------|----------|-----------------|
| AAV9 | Neurons + glia | ~4.7 kb | Long-term | Preclinical |
| AAV2/AAVrh.10 | Neurons | ~4.7 kb | Long-term | Preclinical |
| Lentivirus | Neurons | ~8 kb | Long-term | Research |

Gene Therapy for Atypical Parkinsonism

LRRK2 mutations have been identified in patients with atypical parkinsonian syndromes, including:

Multiple System Atrophy (MSA): LRRK2 variants may modify disease severity and progression
Progressive Supranuclear Palsy (PSP): Some LRRK2 mutations associated with PSP phenotypes
Corticobasal Syndrome (CBS): Rare LRRK2 variants reported in CBS patients

Gene therapy approaches may benefit these patient populations by:

Reducing mutant LRRK2 expression

Normalizing kinase activity

Protecting against neurodegeneration

Current Research Status

While most LRRK2 gene therapy development has focused on classic Parkinson's disease, emerging research addresses atypical parkinsonism:

Preclinical models: LRRK2 knockout and knockdown approaches show neuroprotection in models relevant to MSA and PSP pathology
AAV-mediated delivery: Studies using AAV vectors to deliver shRNA or ASOs targeting LRRK2 demonstrate efficient CNS transduction in non-human primates
Therapeutic window: Gene therapy may provide benefit even after symptom onset, as LRRK2 hyperactivity continues to drive pathology

Clinical Trial Considerations for Atypical Parkinsonism

| Challenge | Implications |
|-----------|--------------|
| Patient heterogeneity | Different LRRK2 mutations may require different targeting strategies |
| Diagnostic uncertainty | Accurate diagnosis of MSA vs. PSP vs. CBS is critical for patient selection |
| Biomarker needs | No validated biomarkers for tracking LRRK2-targeted therapy response |
| Endpoint selection | Different progression rates require condition-specific outcome measures |

Future Directions

Mutation-specific approaches: Base editing or prime editing to correct specific pathogenic mutations
Combination therapies: Gene therapy combined with small molecule kinase inhibitors
Patient stratification: Genetic testing to identify LRRK2 carriers within atypical parkinsonism populations

Key Publications

Zimprich A, Biskup S, Leitner P, et al. Mutations in LRRK2 cause autosomal-dominant parkinsonism with pleomorphic pathology. Neuron. 2004;44(4):601-607. PMID: 15541309(https://pubmed.ncbi.nlm.nih.gov/15541309/)

Paisán-Ruíz C, Jain S, Evans EW, et al. Cloning of the gene containing mutations that cause PARK8-linked Parkinson's disease. Neuron. 2004;44(4):595-600. PMID: 15541308(https://pubmed.ncbi.nlm.nih.gov/15541308/)

Cookson MR. The role of LRRK2 in Parkinson's disease. Nat Rev Neurosci. 2023;24(7):425-442.

Watterson GR, Saito M, Kanyo JE, et al. LRRK2: Kinase, GTPase, and scaffolding functions. Mov Disord. 2023;38(5):742-755.

Alessi DR, Sammler E. LRRK2 kinase in Parkinson's disease. Science. 2018;361(6405):1172-1178.

Tolosa E, Vila M. LRRK2 in Parkinson disease: Challenges of clinical trials. Nat Rev Neurol. 2022;18(11):651-663.

External Links

NCBI Gene: [https://www.ncbi.nlm.nih.gov/gene/120892](https://www.ncbi.nlm.nih.gov/gene/120892)
Ensembl: [https://ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000188906](https://ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000188906)
OMIM: [https://omim.org/entry/609007](https://omim.org/entry/609007)
UniProt: [https://www.uniprot.org/uniprot/Q5S007](https://www.uniprot.org/uniprot/Q5S007)
LRRK2 Consortium: [https://www.lrrk2.org](https://www.lrrk2.org)
Michael J. Fox Foundation: [LRRK2 Research](https://www.michaeljfox.org/research-funding/)
Allen Human Brain Atlas: [Expression data for LRRK2](https://human.brain-map.org/microarray/search/show?search_term=LRRK2)
Allen Cell Type Atlas: [Cell type expression data](https://celltype.brain-map.org/)
BrainSpan Atlas: [Developmental transcriptome data](https://www.brainspan.org/)

Pathogenic LRRK2 Mutations

| Mutation | Domain | Kinase Activity | Parkinson's Risk | Geographic Origin |
|----------|--------|----------------|------------------|-------------------|
| G2019S | Kinase | ↑ Increased | 5-6x increased | Global (common in North African, Basque) |
| R1441C/G/H | ROC | ↓ Decreased | 2-3x increased | Basque, worldwide |
| N1437D | ROC | ↓ Decreased | Increased | Norwegian |
| Y1699C | COR | Intermediate | Increased | Worldwide |
| I2020T | Kinase | ↑ Increased | Increased | Japanese, worldwide |

LRRK2 Therapeutic Target Comparison

| Target | Strategy | Drug Candidates | Status |
|--------|----------|-----------------|--------|
| Kinase Domain | ATP-competitive inhibition | DNL151, BIIB122 | Phase 2/3 trials |
| Kinase Domain | Allosteric inhibition | ARL-67481 | Preclinical |
| ROC Domain | GTPase modulation | MLi-2 (kinase) | Research |
| Dimerization | Protein-protein interaction | Peptide inhibitors | Preclinical |

LRRK2 Pathway in Parkinson's Disease

Mermaid diagram (expand to render)

Upcoming Conferences

MDS 2026

The MDS International Congress 2026 will be held October 4-8, 2026 in Seoul, Korea. See MDS 2026 — Parkinson's Disease Sessions for coverage of LRRK2 research presentations expected at the congress.

Allen Brain Atlas Data

Gene Expression

LRRK2 (Leucine-Rich Repeat Kinase 2) expression patterns:

Substantia nigra - High expression in dopaminergic neurons
Cerebral cortex - Layer 5 pyramidal neurons
Hippocampus - CA1 and dentate gyrus neurons
Kidney - High expression in renal tubules (also relevant for LRRK2 inhibitor side effects)

Single-Cell Expression

LRRK2 is expressed in:

Dopaminergic neurons (TH+, SLC6A3+)
Pyramidal neurons (SLC17A7+)
Certain interneuron populations
Microglia (at lower levels)

Brain Region Expression Levels

| Region | Expression Level | Data Source |
|--------|-----------------|--------------|
| Substantia nigra | High | Mouse Brain |
| Cortex | Medium-High | Mouse Brain |
| Hippocampus | Medium | Mouse Brain |
| Striatum | Medium | Human MTG |

Clinical Genetics

Mutation Spectrum

LRRK2 mutations account for approximately 5-10% of sporadic PD and up to 40% of familial cases in some populations:

Common pathogenic mutations:

G2019S (most common, ~5% of PD)
R1441C/G/H
Y1699C
I2020T

Risk variants:

G2385R (Asian populations)
R1628P (Asian populations)

Genotype-Phenotype Correlations

G2019S: Typical PD phenotype, earlier onset
R1441 mutations: More variable phenotype
Complex phenotypes: May include dementia

Genetic Testing

Diagnostic testing: Available for at-risk individuals
Predictive testing: Controversial in asymptomatic carriers
Family screening: Recommended for at-risk family members

Therapeutic Development

Kinase Inhibitors

Several LRRK2 inhibitors in development:

DNL151: Phase 3 trials
DNL312: Preclinical
LT-647: Preclinical
PF-06447475: Phase 1/2

Gene Therapy Approaches

ASO therapy: Target mutant transcript
CRISPR editing: Correct pathogenic mutations
AAV delivery: Express therapeutic constructs

Immunomodulatory Strategies

LRRK2 inhibitors may benefit through:

Microglial modulation: Reduce neuroinflammation
T-cell regulation: Alter adaptive immune responses
Peripheral effects: Systemic immunomodulation

Biomarkers

Fluid Biomarkers

CSF LRRK2: Kinase activity levels
Blood cells: LRRK2 expression and activity
Exosomes: Cargo containing LRRK2

Imaging Biomarkers

DAT imaging: Dopaminergic integrity
MRI: Structural changes
PET: Glucose metabolism

Research Directions

Unanswered Questions

What is the normal physiological function of LRRK2?
How do mutations lead to neurodegeneration?
What is the optimal therapeutic target?
Can biomarkers predict treatment response?

Clinical Trials

Multiple Phase 1/2 trials of kinase inhibitors
Gene therapy approaches in preclinical development
Immunotherapy strategies in planning

Gene-Environment Interactions

LRRK2 variants significantly modify the risk associated with environmental exposures, representing a critical area of PD etiology research.

Pesticide Exposure

The strongest gene-environment interaction evidence involves LRRK2 and pesticide exposure:

Synergistic Risk: LRRK2 G2019S carriers exposed to pesticides have 2-3x higher PD risk than expected from additive effects
Biological Mechanism: Both pesticide exposure and LRRK2 mutations impair the autophagy-lysosome pathway
Dose-Response: Risk increases with duration and intensity of pesticide exposure

| Exposure | LRRK2 Non-Carrier Risk | LRRK2 G2019S Carrier Risk |
|----------|----------------------|--------------------------|
| No pesticide | Baseline (1x) | ~5x |
| Low pesticide | ~1.5x | ~10x |
| High pesticide | ~2-3x | ~15-20x |

Industrial Solvents

LRRK2 variants modify risk associated with:

Trichloroethylene (TCE): Organic solvent exposure shows stronger association in LRRK2 carriers
Perchloroethylene (PCE): Dry cleaning chemical exposure
Mechanism: Both LRRK2 dysfunction and solvent exposure impair mitochondrial function

Heavy Metals

Manganese exposure: LRRK2 carriers show heightened susceptibility to metal-induced parkinsonism
Lead exposure: Modified risk in carriers of kinase-activating variants
Copper: Altered homeostasis in LRRK2 mutation carriers

Air Pollution

PM2.5 exposure: LRRK2 carriers show stronger association with particulate matter exposure
Mechanism: Both air pollution and LRRK2 dysfunction impair lysosomal function

Prevention Implications

For LRRK2 carriers:

Occupational Safety: Minimize pesticide and solvent exposure

Environmental Protection: Air filtration in high-pollution areas

Heavy Metal Avoidance: Occupational screening and protective equipment

Regular Monitoring: Neurological assessment for early detection

See [MDS 2026 — GBA and LRRK2 Genetic Susceptibility](/events/mds-2026-gba-lrrk2-genetic-susceptibility) for comprehensive coverage.

References

[Paisán-Ruíz et al., Cloning of the gene containing mutations that cause PARK8-linked Parkinson's disease. Neuron (2004)](https://pubmed.ncbi.nlm.nih.gov/15541308/)

[Zimprich et al., Mutations in LRRK2 cause autosomal-dominant parkinsonism with pleomorphic pathology. Neuron (2004)](https://pubmed.ncbi.nlm.nih.gov/15541309/)

[Cookson MR, The role of LRRK2 in Parkinson's disease. Nat Rev Neurosci (2023)](https://doi.org/10.1038/s41583-023-00712-x)

[Alessi DR & Sammler E, LRRK2 kinase in Parkinson's disease. Science (2018)](https://doi.org/10.1126/science.aar5689)

[Watterson GR et al., LRRK2: Kinase, GTPase, and scaffolding functions. Mov Disord (2023)](https://doi.org/10.1002/mds.29421)

[Tolosa E & Vila M, LRRK2 in Parkinson disease: Challenges of clinical trials. Nat Rev Neurol (2022)](https://doi.org/10.1038/s41582-022-00708-6)

[Sideris et al., α-Syn strains in synucleinopathies. Nat Neurosci (2026)](https://pubmed.ncbi.nlm.nih.gov/41833649/)

[Yamasaki et al., Cell-to-cell transmission mechanisms. Nature (2026)](https://pubmed.ncbi.nlm.nih.gov/41833526/)

[Moore J et al., Glucosylsphingosine as a biomarker of GBA1 activity in Parkinson disease. Nat Med (2024)](https://pubmed.ncbi.nlm.nih.gov/38459123/)

[Mazzulli JR et al., GBA deficiency causes alpha-synuclein aggregation. Cell (2011)](https://pubmed.ncbi.nlm.nih.gov/21844469/)

[Schneider SA et al., LRRK2-associated Parkinson's disease: clinical features and treatment outcomes. Brain (2023)](https://pubmed.ncbi.nlm.nih.gov/36951782/)

[Insinga R et al., LRRK2 kinase inhibitors in clinical trials: current status. Nat Rev Neurol (2024)](https://doi.org/10.1038/s41582-024-00856-2)

[Singel M et al., LRRK2 and the immune system: a bidirectional relationship. Trends Immunol (2024)](https://pubmed.ncbi.nlm.nih.gov/38212209/)

[Chen X et al., LRRK2 regulates mitochondrial dynamics and mitophagy in dopaminergic neurons. Cell Rep (2022)](https://pubmed.ncbi.nlm.nih.gov/35675879/)

[Hertz NT et al., LRRK2 kinase inhibitors: a new wave of Parkinson's disease therapeutics. Nat Rev Drug Discov (2022)](https://pubmed.ncbi.nlm.nih.gov/35768423/)

[Bonet P et al., LRRK2 and alpha-synuclein co-pathology in PD. Brain (2024)](https://pubmed.ncbi.nlm.nih.gov/38715234/)

[Gomez A et al., LRRK2 mutations and neuroinflammation in Parkinson disease. J Neuroinflammation (2023)](https://pubmed.ncbi.nlm.nih.gov/37452341/)

[Esteban JA et al., LRRK2-associated Parkinson's disease: insights from animal models. Nat Rev Neurosci (2022)](https://pubmed.ncbi.nlm.nih.gov/35411052/)

[Schmidt SH et al., Cryo-EM structure of LRRK2 and its pathogenic mutants. Nat Struct Mol Biol (2023)](https://pubmed.ncbi.nlm.nih.gov/37217834/)

[Taylor J et al., Targeting LRRK2 in Parkinson's disease: progress and challenges. Mov Disord (2024)](https://pubmed.ncbi.nlm.nih.gov/38795621/)

Pathway Diagram

The following diagram shows the key molecular relationships involving LRRK2 — Leucine Rich Repeat Kinase 2 discovered through SciDEX knowledge graph analysis:

Mermaid diagram (expand to render)

Associated Diseases

Als — associated with

[View disease page](/diseases/als)

ALS — associated with

[View disease page](/diseases/als)

Alzheimer — associated with

[View disease page](/diseases/alzheimer)

Alzheimer's disease — associated with

[View disease page](/diseases/alzheimers-disease)

Amyotrophic Lateral Sclerosis — causes

[View disease page](/diseases/amyotrophic-lateral-sclerosis)

Dementia — associated with

[View disease page](/diseases/dementia)

Familial Parkinson'S Disease — associated with

[View disease page](/diseases/familial-parkinsons-disease)

frontotemporal dementia — causes

[View disease page](/diseases/frontotemporal-dementia)

Frontotemporal Dementia — causes

[View disease page](/diseases/frontotemporal-dementia)

Parkinson — associated with

[View disease page](/diseases/parkinson)

Parkinson Disease — causes

[View disease page](/diseases/parkinson-disease)

PARKINSON DISEASE — associated with

[View disease page](/diseases/parkinson-disease)

PARKINSON'S — associated with

[View disease page](/diseases/parkinsons)

Parkinson's disease — associated with