Models for Preclinical Parkinson's Disease Research

Parkinson's disease (PD) is multifactorial, demanding investigation across multiple mechanisms and presenting unique preclinical research challenges. JAX's validated PD models and services are built to meet them.

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The Jackson Laboratory - Models for Preclinical Parkinson's Disease Research

In Vivo Parkinson's Disease Models

JAX's portfolio of translatable PD models is organized by key gene targets to help you identify the best model for your research.
View the JAX Suite of Parkinson's Disease Models in the JAX Repository

Gba1

Common Name	Phenotype	Disease Latency	Details
Gba D409V KI (019106) KI & Floxed	Homozygous mice show a significant reduction in Gba1 protein level and glucocerebrosidase activity, and a significant increase in glucosylsphingosine in both brain and liver tissues	8 months	Cognitive & motor impairment by the age of 12 months High levels of soluble monomeric α-synuclein in the hippocampus at 12 months

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LRRK2

Common Name	Phenotype	Disease Latency	Details
BAC Lrrk2-G2019S (012467) Transgenic	Age-associated decrease in striatal dopamine by 12 months No loss of dopaminergic neurons or behavioral motor deficits	3 months	Mitochondrial abnormalities & neuroinflammation by 3 months Motor impairment by 18 months
BAC LRRK2 (G2019S) (018785) Transgenic	Altered glutamatergic synaptic transmission in midbrain DA neurons by 12 months	5 months (females)	LRRK2 G2019S expression exacerbates PFF-mediated α-syn aggregation and degeneration pathology in mice Hyperlocomotion and increased exploratory behavior by 12 months in males and by 5 months in females

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Ndufs2

Common Name	Phenotype	Disease Latency	Details
cNdufs2^- (MCI-Park) (036313) Conditional KO	Progressive neural and behavioral decline, with mild deficits starting after around postnatal day 30 and becoming overt by day 100 Mitochondrial abnormalities, dopamine deficiency & neuronal loss by 3 months	2 months	Motor deficits by 3 months By age 60 days, TH expression decreases in substantia nigra dopaminergic neurons Survival less than 6 months

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Parkin

Common Name	Phenotype	Disease Latency	Details
Parkin KO (006582) KO	Mitochondrial abnormalities & dopamine deficiency by 3 months	3 months	Motor deficits by 5 months

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Pink1

Common Name	Phenotype	Disease Latency	Details
Pink1 KO (017946) KO	Mitochondrial abnormalities by 3 months	2 months	Reduced spontaneous locomotor activity and skill reported at 3-6 months

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SNCA

Common Name	Phenotype	Disease Latency	Details
Snca^-; PAC-Tg(SNCA^WT) (010710) KO & Transgenic	No phenotype	N/A	Experimental control mice for strains that model the early gastrointestinal dysfunction in the absence of major central nervous system pathology seen in human Parkinson's disease
Snca^-; dbl-PAC-Tg(SNCA^A53T) (010799) KO & Bitransgenic	Gastrointestinal dysfunction by 3 months	2 months	Neurons in the enteric nervous system develop α-synuclein pathology Neurons in the brain are spared: no evidence of dopaminergic neuron loss Motor impairment by 6 weeks
A53T α-synuclein transgenic line M83 (004479) Transgenic	Homozygous mice develop a progressively severe motor phenotype	8 months	Alpha-synuclein inclusions, with dense accumulation in the spinal cord, brainstem, cerebellum and thalamus by 8-12 months Impaired odor discrimination at 6 months
mThy1-hSNCA line 15 (017682) Transgenic	Progressively increasing expression of human αSyn starting at 4 weeks	1 month	Proinflammatory gut microbiome at 2 months
Hualpha-Syn(A53T) transgenic line G2-3 (006823) Transgenic	Age-dependent phenotype including progressive motor deficits, intraneuronal inclusion bodies and neuronal loss	N/A	Clinical abnormalities by 10 months Astrocytosis in the midbrain, deep cerebellar nuclei, brainstem and spinal cord Abnormal neuronal accumulations of α-Syn & ubiquitin by 4 months Loss of dopaminergic neurons
Line 61 (mThy1 hα-syn Tg) (038796) Transgenic	Alpha-synuclein inclusions by 1 month Mitochondrial abnormalities by 4 months Progressive dopamine deficiency in the striatum starting at 14 months	1 month	Motor impairments as early as 1 month Neuroinflammation in the striatum (1 month) and the substantia nigra (5-6 months) Non-motor impairments by 3 months
hm²α-SYN-39 (008239) Transgenic	Progressive impairment in motor function	2 months	Neuroinflammation starting at 1 month Abnormalities in the dopaminergic system, including low dopamine levels and difficulties with motor coordination (13 months)

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FAQs for Parkinson’s Disease Mouse Models

What are the different types of preclinical Parkinson’s disease models and how are they used in research?

How do genetic targets like LRRK2, GBA1, SNCA, and PINK1 influence Parkinson’s disease models?

How do researchers choose the right Parkinson’s disease mouse model based on phenotype, disease latency, and study goals?

Series of Gene Replacement Models for PD

Explore JAX's currently available gene replacement models for neurodegenerative diseases. Gene replacement models are often considered more physiologically relevant, as the entire mouse gene is replaced with the human gene under endogenous control. These models typically exhibit expression levels and patterns that more closely reflect physiological conditions.

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