General Information

Mouse: C57BL/6 x 129/SvEvBrd

Mice in which exons 4-5 of the PINK1 gene have been deleted by insertion of a neo probe (PGK-neo-pA) using homologous recombination. This insertion removes the N-terminal portion of the PINK1 protein that contains the kinase activity causing loss of function.

Corresponding human genotype: Autosomal recessive mutation in the PINK1 gene causing a loss-of-function of the protein and leading to early-onset Parkinson’s disease (PARK6).

Mutated gene: PINK1

References: Akundi 2011

Loss of dopaminergic neurons

  • 12 months: apparent reduction in the number of TH-positive neurons in the SN. This decrease is accompanied by an increase of phosphorylated c-Jun protein in dopaminergic neurons.

Dopamine Homeostasis

  • 2 months: no changes in dopamine levels and dopamine turnover are detected in the striatum
  • 612 months: reduction of dopamine levels in the striatum (levels are about 75% those measured in wild type mice). An increase in dopamine turnover is detected in the striatum.


  • Not reported

Motor Behaviours

  • Not reported

Response to dopaminergic treatment

  • Not reported

Non motor Behaviours

  • Not reported


  • Not reported


6 months: increased levels of cytokine (IL-1beta, IL-10 and IL-12) in the striatum in response to a peripheral inflammatory stimuli (LPS) suggesting an enhanced susceptibility to inflammation.

3 thoughts on “mPINK1 KO/2 (Pink1-/-) – Mouse

    1. parkinsonuser Post author

      To get more information on the availability of the model you should contact the laboratory that created it. A link to the publication can be found under “references” in the General information section.


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