This website is now the new JPND's archival platform. This website hosts all of JPND's archived content and resources.
Please continue to visit this site to access publications, videos and reports from JPND's activities.
General Information
Mice: C57BL/6
Expression of the full-length human LRRK2 protein under the control of the mouse Thy1-regulatory sequences.
Endogenous LRRK2: yes
Corresponding human genotype: LRRK2 is the greatest known genetic contributor to Parkinson’s disease.
Targeted gene: LRRK2
References: Herzig-2012
Transgene expression
- 5-7 months: The human transgene is expressed in the striatum, cortex, hippocampus, and brainstem but not detectable in the SN and cerebellum.
Neurodegeneration
- Up to 19 months: No obvious neurodegeneration is observed.
Dopamine Homeostasis
Not reported
Inclusions
- Up to 15 months: No differences in the levels of alpha-synuclein (phosphorylated or not) or Tau (phosphorylated or not) are observed in the brain of transgenic animals.
Motor Behaviours
- 3-10 months: The transgenic animals seem to perform slightly better on the accelerating rotarod compared to control littermates, however, the effect is only seen at a young age (3-4 months) and is not significant.
Response to dopaminergic treatment
- Not reported
Non-motor Behaviours
- 2-4 months: No difference is observed in term of anxiety or learning abilities (open field, the dark/light box, elevated plus-maze or Morris water maze).
Electrophysiology
- Not reported
Neuroinflammation
- 6-12 months: No difference in the number of glial cells is observed.
