Explore Taconic's portfolio of Parkinson's disease models and learn how our strategic partnership with the Michael J. Fox Foundation drives groundbreaking research. Discover the advanced tools and resources available to accelerate your Parkinson's disease studies.
The Michael J Fox Foundation Sponsored Rats for Parkinson's Research
The loss of nigrostriatal dopamine neurons and reduced motor abilities are consequences of Parkinson's Disease. Mutations in the LRRK2 and alpha synuclein (SNCA) genes are associated with familial Parkinson's disease and affect the nigrostriatal pathway.
The rat as an experimental organism can offer some unique strengths compared to mice:
- rats can perform more sophisticated behavioral tasks,
- are better suited for electrophysiological multichannel recordings, and
- the nigrostriatal circuit of the rat is more sensitive to insults than that of mice.
aSyn SNCA KO Rat
The aSyn SNCA Knockout Rat (Model 22966) is a valuable model for Parkinson’s Disease (PD) research. Originally generated at SAGE Labs and now available through Taconic as of April 2025, this model uses CRISPR/Cas9 to delete the endogenous SNCA gene and enables targeted study of alpha-synuclein’s role in neurodegeneration.
aSyn A53T SNCA KI Rat
The aSyn A53T SNCA Knock-In Rat (Model 22964) supports Parkinson’s Disease (PD) research by replicating a key human SNCA mutation linked to both familial and sporadic forms of the disease. Created using CRISPR/Cas9 and first available through Taconic in April 2025, the aSyn A53T SNCA Knock-In Rat expresses a humanized A53T-mutated alpha-synuclein protein, with the endogenous rat SNCA gene rendered nonfunctional.
The Floxed Prkn Mouse
Model 21546 is a conditional knock-out of the PRKN gene.
- This strain contains a conditional Prkn allele in which exon 7 is floxed
- The PRKN gene may be deleted in a tissue - or temporal-specific manner using viral delivery of Cre recombinase
- Mutations in the homologous PRKN gene are associated with early-onset Parkinson's disease in humans
More Parkinson's Rat Models Sponsored by The Michael J Fox Foundation
- Human Alpha Synuclein A53T Rat
- Human Alpha Synuclein E46K Rat
- Human Alpha Synuclein Rat
- Human LRRK2 G2019S Rat
- hTH-GFP Rat (X-linked)
- hTH-GFP Rat (Autosomal Insertion)
- Human LRRK2 R1441G Rat*
*Discontinued. Please contact Taconic if you need this line.
Additional Taconic Parkinson's Disease Models
The Rab29 Overexpression Mouse
Model 16552 is a constitutive knock-in of murine Rab29 under control of the Pgk promoter generated by targeted transgenesis into the ROSA26 locus.
- Rab29 is a Rab GTPase that acts as a key regulator in vesicle trafficking and maintaining the endosome-trans-Golgi network structure. Rab29, together with LRRK2, plays a role in the retrograde trafficking pathway for recycling proteins.
- Rab29 is one of five genes located within the PARK 16 locus that has been linked to Parkinson's disease.
- Rab 29 is a direct substrate of LRRK2 — a kinase protein in which autosomal dominant missense mutations are linked to Parkinson's disease through increased kinase activity. In addition, Rab29 is a regulator of LRRK2, controlling its localization and activation.
- There is a substantial increase in Rab29 protein levels by western blot in brain, kidney, and distal colon, with a moderate increase in spleen, lungs, macrophages.
The Human LRRK2 G2019S Targeted Replacement Mouse
Model 13940 has the human G2019S point mutation introduced into exon 41 of the mouse LRRK2 gene. Additionally, exon 41 is flanked by lox P sites, potentially allowing generation of a LRRK2 gene constitutive KO model upon intercrossing with a Cre-deleter strain. See model page for more information.
- The G2019S alpha-mutation is linked to the development of Parkinson's disease, both sporadic and familial.
- In patients, the G2019S LRRK2 mutation is an autosomal dominant mutation that leads to pathology similar to what is observed with idiopathic Parkinson's disease.
- At 18 months of age, LRRK2 G2019S mice show an increased locomotor response after amphetamine challenge.
- This knock-in mutation does not appear to affect basal motor function or more complex behavior in C57Bl6 mice.
What our customers say:
“Robust, well-validated pre-clinical models of Parkinson's disease are a necessary tool for understanding the biology and possible treatment of this complex disease. With dedicated project management and technical support, Taconic has been a reliable partner in The Michael J. Fox Foundation's efforts to provide the research community with important, field-enabling pre-clinical models. We look forward to continuing to partner with Taconic for custom model generation projects.”
The Michael J. Fox Foundation
