AI Article Synopsis
- - Mutations in the PRKN gene are a leading cause of autosomal recessive Parkinson's disease (PD), but research on parkin-/- mice shows no early loss of dopaminergic neurons or motor symptoms.
- - This study focused on how the absence of the parkin gene affected the retina's mitochondria and synaptic structures in 6-month-old mice, revealing a thicker retina and significant mitochondrial abnormalities.
- - The findings indicate that parkin-/- mice experienced impaired mitochondrial function and structural changes in the retina, which disrupted communication between photoreceptors and retinal neurons, leading to visual impairment.
Article Abstract
Mutations in the PRKN gene are the major cause of autosomal recessive Parkinson's disease (PD). However, studies of parkin-/- mice did not show the loss of dopaminergic neurons and motor phenotypes at a young age. Whether pathological changes are associated with nonmotor symptoms of PD remains unclear. Visual impairment is one common nonmotor symptom in patients with PD. This study aimed to examine the effects of parkin-/- on mitochondria and synaptic structures in the retina of 6-month-old mice. Compared with wild-type mice, parkin-/- mice exhibited a slightly thickened retina. Also, the number of normal mitochondria (mito-5 grade) in rod spherules (RSs) significantly decreased (p < 0.01), the average area of mitochondria was significantly larger (p < 0.001), and the number of ribbons in RSs significantly decreased (p = 0.02). The RSs of parkin-/- mice showed severe swelling after flicker stimulation. Our study implicated that parkin-/- led to the impairment of mitochondria and abnormality of the synaptic structure in mouse retina at a young age, which damaged the synaptic transmission between photoreceptors and second-order retinal neurons and resulted in visual impairment.
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| http://dx.doi.org/10.1016/j.neulet.2022.136888 | DOI Listing |
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