Аннотация:Parkinson's disease (PD), characterized by loss of nigrostriatal dopaminergic neurons, is diagnosed by the appearance of motor disorders many years after the onset of
neurodegeneration, which explains low efficiency of treatment. The only hope to improve the treatment is the development of preclinical diagnosis, based on searching
biomarkers as changes in premotor functions. Since impaired visual function is among PD manifestations, this study aimed to search for biochemical changes in the eye
of mice when modeling preclinical (presymptomatic) and clinical (symptomatic) stages of PD using neurotoxin MPTP. The mRNA level and protein content of tyrosine
hydroxylase (TH) were assessed in the retina using realtime PCR and Western blot. In addition, the concentration of catecholamines was measured in the retina and
iridociliary complex by HPLC. Presymptomatic mice show the increased levels of dopamine and metabolites in retina. Apparently, this is due to a compensatory
increase in TH activity, since the TH protein content remains at the control level. Symptomatic mice show an abrupt decrease in the TH protein content, whereas the
retinal dopamine content remains at the control level. This observation is also a manifestation of a compensatory reaction. The above data suggest that compensatory
changes observed in the retina are similar to those previously found in the substantia nigra in these animal models. In the iridociliary complex, a decrease in the
norepinephrine concentration was found in symptomatic mice, which may be due to a degradation of noradrenergic neurons innervating the iris and ciliary body.
Changes found in parkinsonian animals correlate well with clinical data that the reaction of the pupil is slowed and the incidence of glaucoma is increased in PD patients.
Thus in presymptomatic mice, pathological processes extend to the eye, followed by changes in the tear fluid and intraocular pressure, which can serve as preclinical
diagnostic markers.