Abstract
Parkinson's disease (PD) is a systemic neurodegenerative condition caused by the death of dopaminergic neurons of the nigrostriatal system of the brain. This disease is diagnosed after most neurons have already been lost, which explains the low efficiency of treatment. Hope for increasing treatment efficiency rests in the development of new strategies for early diagnosis of PD based on a search for peripheral markers that appear as early changes in non-motor functions. Since impairment of the visual function is one of the manifestations of PD, the purpose of our work was to identify biochemical and physiological changes in a mouse's eye and eyelid in models of preclinical (presymptomatic) and clinical (symptomatic) stages of PD. We found that the norepinephrine, dopamine, and serotonin levels in the mouse eye reduced not only in the model of the early clinical stage, but also in the model of preclinical stage, an indication that pathological changes in the monoaminergic systems of the brain had affected the eye even before the motor disorders emerged. Moreover, in both models of PD, mice had increased intraocular pressure, indicating the development of both metabolic and functional impairments, which can be used as diagnostic markers. Unlike in the eye, the serotonin level in the eyelid was increased in mice at both parkinsonism stages and in presymptomatic mice to a much higher extent than in symptomatic ones. Given that serotonin is involved in the regulation of lacrimal glands of the eyelid, an increase in its level in parkinsonian mice should alter the composition of tear fluid, which could serve as a diagnostic marker of early stage of PD. Thus, the changes in the metabolism of monoamines in the eye and eyelid observed in mice at the early stage of parkinsonism are accompanied by changes in the function of these structures and, therefore, can be used as diagnostic markers of the early stage of PD.
Highlights
Parkinson’s disease (PD) is a widespread neurodegenerative disorder caused by the degeneration of the nigrostriatal system of the brain, the key element in the regulation of the motor function
A 48.2% decrease in the total distance was observed in the model of the early clinical stage of PD compared to the control after MPTP administration (Table)
Characterization of the experimental model of Parkinson’s desease An important feature of PD is that it has an estimated threshold of neurodegeneration at which motor symptoms occur, meaning the disease proceeds from the preclinical to the clinical stage
Summary
Parkinson’s disease (PD) is a widespread neurodegenerative disorder caused by the degeneration of the nigrostriatal system of the brain, the key element in the regulation of the motor function. There is a pressing need for developing early (preclinical) diagnosis of PD long before the appearance of motor symptoms, as this could make it possible to use neuroprotective therapy to slow down or even stop neurodegeneration [1]. The existing approach to the development of early diagnosis of PD is based on the idea that the disease is systemic; its non-motor symptoms caused by the impaired function of both brain regions beyond the nigrostriatal system and the peripheral nervous system appear long before the motor disorders [1, 2]. It is assumed that complex preclinical diagnosis of PD can be developed on the basis of early changes in non-motor functions and the corresponding changes in body fluids (cerebrospinal fluid and blood) [1]
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