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Genetically modified rodent models have been valuable for investigating the pathogenesis of neurodegenerative diseases such as Parkinson’s disease (PD). Based on the fact that mutations in the  PINK1  gene cause autosomal recessive juvenile parkinsonism, a number of mouse models with deletion of the  PINK1  gene were generated. However, these  PINK1  knockout mouse models fail to recapitulate the selective and overt neurodegeneration seen in PD patient brains. Recently, we generated a non-human primate model with  PINK1  deletion using CRISPR/Cas9. This monkey model shows robust neurodegeneration in various brain regions, different from late-onset neurodegeneration in PD patients. Because of the limited pathological data available from humans carrying PINK1 mutations, the PINK1 mutant monkeys provide us with an important animal model to discuss the unique function of PINK1 that is essential for neuronal survival in primate brains. We also propose that the impairment of this unique function by  PINK1  mutations in humans may account for the age-dependent and progressive neurodegeneration.

A CRISPR monkey model unravels a unique function of PINK1 in primate brains