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Neurodegenerative Disease Models

Parkinson Mouse Model

Since 1998, ingenious targeting laboratory has supported Parkinson disease research with custom mouse models enabling mechanistic studies of dopaminergic neurodegeneration, evaluation of neuroprotective strategies, and preclinical testing of disease modifying therapeutics.

Parkinson disease mouse models provide essential platforms for investigating the molecular pathways underlying neuronal loss in the substantia nigra, testing hypotheses about alpha synuclein aggregation and spread, and developing therapies targeting LRRK2, GBA, and other genetically validated targets.

2,500+
Projects Completed
800+
Publications
26+
Years Experience
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Genetic Basis of Parkinson Disease

Parkinson disease results from progressive loss of dopaminergic neurons in the substantia nigra, leading to characteristic motor symptoms including tremor, rigidity, and bradykinesia. While most cases are sporadic, genetic studies have identified numerous loci associated with familial and sporadic disease risk.

SNCA (Alpha Synuclein)

Point mutations (A53T, A30P, E46K) and gene multiplications cause autosomal dominant Parkinson disease. Alpha synuclein aggregation into Lewy bodies is a pathological hallmark.

LRRK2

The G2019S mutation is the most common genetic cause of Parkinson disease. Increased LRRK2 kinase activity is implicated in both familial and sporadic disease.

PARK2, PINK1, DJ1

Recessive mutations cause early onset parkinsonism. These genes function in mitochondrial quality control and mitophagy pathways.

GBA

Heterozygous GBA mutations are the most common genetic risk factor for sporadic Parkinson disease, increasing risk approximately fivefold.

Model Types for Parkinson Disease Research

Alpha Synuclein Models

  • SNCA Point Mutation Knockin (A53T, A30P, E46K)
  • SNCA Overexpression Transgenic
  • SNCA Knockout
  • Conditional SNCA Models

LRRK2 Models

  • LRRK2 G2019S Knockin
  • LRRK2 Kinase Dead Knockin
  • LRRK2 Knockout
  • LRRK2 R1441C/G Knockin

Mitochondrial Pathway

  • Parkin (Park2) Knockout
  • PINK1 Knockout
  • DJ1 (Park7) Knockout

GBA Models

  • GBA Point Mutation Knockin (N370S, L444P)
  • Conditional GBA Knockout

Cell Type Specific Approaches

Parkinson disease selectively affects specific neuronal populations. Conditional approaches target relevant cell types.

Dopaminergic Neuron Targeting

DAT Cre or TH Cre

Catecholaminergic neurons; DAT Cre more restricted to dopaminergic neurons

Regional Specificity

En1 Cre or Pitx3 Cre

Midbrain dopaminergic neurons from early development

Temporal Control

DAT CreERT2

Gene manipulation in adult dopaminergic neurons, avoiding developmental compensation

Phenotyping Parkinson Disease Models

Motor Assessment

Open Field

Spontaneous locomotor activity, rearing, and movement patterns

Rotarod

Motor coordination and balance with accelerating protocols

Pole Test

Bradykinesia assessment; time to descend correlates with dopaminergic function

Gait Analysis

Stride length, cadence, and coordination; automated systems available

Cylinder Test

Forelimb asymmetry in unilateral lesion models

Neuropathology Endpoints

  • Dopaminergic neuron counts: Stereological quantification of TH positive neurons in substantia nigra
  • Striatal dopamine: HPLC measurement of dopamine and metabolites
  • Synuclein pathology: Phospho synuclein (Ser129), aggregated synuclein, Lewy body like inclusions
  • Neuroinflammation: Microglial activation (Iba1), astrogliosis (GFAP), and inflammatory markers

Selected Publications in Parkinson Disease Research

Recent publications demonstrate the utility of genetically engineered mouse models in Parkinson disease research:

What Researchers Say

ingenious Targeting Laboratory is highly recommended for generating custom animal models. Past 2 years, we have made 2 conditional knockout mouse lines. All processes of each project were scientifically and professionally handled. Their scientific consulting to initiate the project was superb compared to other companies, and transparency of the project progress reported by project managers was excellent. Their excellency and dedication to meet our needs in a timely manner are invaluable to continuation of our research progress.

Hyekyung Plumley, PhD

Warren Center for Neuroscience Drug Discovery

Start Your Parkinson Model Project

Our scientific consultants are ready to discuss your Parkinson disease research requirements and recommend the optimal model design for your program. Initial consultation is provided at no charge.

✦ New for 2026

Breeding Scheme Architect

Plan complex multi-allele breeding strategies, calculate expected genotype ratios, and estimate time to experimental cohorts—all before starting your project.

Visualize multi-generation breeding paths
Calculate Mendelian ratios automatically
Estimate timeline to study-ready cohorts

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Allele 1Gene-flox (conditional)
Allele 2Cre-driver (tissue-specific)
TargetHomozygous knockout

→ 3 generations to target genotype

Frequently Asked Questions

Common PD mutations include SNCA (alpha synuclein) mutations (A53T, A30P, E46K), LRRK2 mutations (G2019S, R1441C/G), PINK1 mutations, and Parkin mutations. Point mutation knockins can introduce any specific human mutation for disease modeling at physiological expression levels.

Standard motor assessments include rotarod (motor coordination), pole test (bradykinesia), open field (locomotor activity), gait analysis (stride length, coordination), and cylinder test (forelimb asymmetry in unilateral models). Dopaminergic neuron counts in substantia nigra and striatal dopamine levels are key pathological endpoints.

Yes. Conditional expression of PD mutations (e.g., Cre dependent SNCA or LRRK2 mutations) enables temporal and spatial control, allowing study of dopaminergic neuron specific effects or adult onset disease. This can avoid developmental defects and better model sporadic versus familial PD.

Disease progression varies by mutation and model type. SNCA transgenic models show motor deficits and synuclein pathology with faster progression than knockin models. LRRK2 models may show slower progression. Knockin models at physiological expression levels typically show more gradual progression than transgenic models with overexpression. Contact us to discuss model selection for your study timeline.

C57BL/6 is most commonly used for Parkinson's models due to extensive characterization, good motor performance, and behavioral baseline data. Strain background can affect dopaminergic function and motor phenotypes, so maintaining consistent backgrounds is important for reproducible experiments.

Lab Signals

Parkinson's Disease Research Insights

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