Deletion of exons 4–7 |
Unchanged DA numbers and levels of striatal DA/DA receptor |
N/A |
N/A |
Striatal plasticity impairments; Increased excitatory transmission |
Feligioni et al., 2016; Kitada et al., 2007 |
Germline deletion |
N/A |
Impaired mitochondrial respiration in striatum; Increased larger mitochondria |
N/A |
Reduced aconitase activity |
Gautier et al., 2008 |
Deletion of exons 4–5 |
Loss of DA neurons in striatum; impaired DA release |
Altered mitochondrial calcium storage |
N/A |
Aberrant innate immune response |
Akundi et al., 2011 |
Deletion of exons 2–3 |
No DA neuronal neurodegeneration |
Increased mitochondrial fragmentation |
No motor deficits observed |
Serotonergic neuronal loss |
Glasl et al., 2012
|
G309D-PINK1 mutation |
Deficiency of striatal DA, no neurodegeneration |
Increased mitochondrial dysfunction with impaired mitochondrial fission |
Reduction of locomotor activity |
Absence of Lewy bodies in SNpc |
Gispert et al., 2009 |
Deletion of exon 1 |
N/A |
Fragmentation of mitochondria; Increased ROS level; Impaired mitochondrial ATP synthesis |
N/A |
Impaired calcium homeostasis |
Oliveras-Salvá et al., 2014 |
Deletion of exons 2–3 |
Reduction of DA in SNpc with neurodegeneration |
Increased mitochondrial stress |
Impaired motor abilities |
N/A |
Moisoi et al., 2014 |