[Signs of anhedonia and destructive changes in the ventral tegmental area of the midbrain in the model of the preclinical Parkinson's disease stage in experiment].

Parkinson's disease (PD) is one of incurable socially significant diseases. Success in the PD treatment is associated with the development of the technology of preclinical diagnosis and neuroprotective treatment of the disease. In the experimental model of the preclinical PD stage in rats created by intranasal administration of the proteasome inhibitor lactacystin, signs of depression as an anhedonia symptom were detected for the first time.

[Study of age changes in compensatory processes on the model of neurodegeneration of nigrostriatal system in rats.].

It is generally accepted that advanced age is the main risk factor for the development and progression of Parkinson's disease (PD). However, data that experimentally confirm the dependence on the age of the rate of neurodegeneration progression and the activity of compensatory processes in the nigrostriatal system in the development of PD are absent in the modern literature. The present study uses a model of neurodegeneration of the nigrostriatal system in rats of different age groups, created by the microinjections of the proteasome inhibitor lactacystin (LC) into the substantia nigra pars compacta (SNpc).

New HSF1 inducer as a therapeutic agent in a rodent model of Parkinson's disease.

Molecular chaperone HSP70 (HSPA1A) has therapeutic potential in conformational neurological diseases. Here we evaluate the neuroprotective function of the chaperone in a rat model of Parkinson's disease (PD). We show that the knock-down of HSP70 (HSPA1A) in dopaminergic neurons of the Substantia nigra causes an almost 2-fold increase in neuronal death and multiple motor disturbances in animals.

[EFFECT OF QUERCETIN ON NEURODEGENERATIVE AND COMPENSATORY PROCESSES IN NIGROSTRIATAL SYSTEM IN A MODEL OF PRECLINICAL PARKINSON''S DISEASE STAGE IN RATS].

Data on HSP70 involvement in Parkinson's disease (PD) pathogenesis, received in last 10 years, cannot answer the question whether the decrease in stress-inducible Hsp70 brain expression is one of the reasons for progressive neurodegeneration in PD. In the present study, the inhibitor of HSPs expression quercetin was used in a rat model of nigrostriatal system proteasome dysfunction. This model was created by the microinjections of the specific proteasome activity inhibitor lactacystin, that was injected locally to the substantia nigra pars compacta (SNpc).