Systemic administration of PRP-1 possesses neuroprotective effects and can prevent the neurodegeneration in hippocampus induced by Abeta25-35. This suggests that PRP-1 could be a potential therapeutic agent for specific neurodegenerative diseases.

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Neurodegenerative diseases are going to increase as the life expectancy is getting longer. Most patients with neurodegenerative diseases (ND) complain of pain, the origin of which remains largely unknown and requires further research. One of the reasons why the topic of pain and PD is difficult to address is that it is sometimes tough to discern whether a particular pain is due to PD or not. Chronic pain is such a common symptom among the general population, and people with PD are not immune to common problems as well. However, there are aspects of PD that may exacerbate the pain experienced from a common problem. In addition, there are particular types of pain that may be unique to people with PD. There is a frequent and more intense onset of pain in Parkinson’s disease, as the most important non-motor symptom, with a violation of both the emotional measurement of pain and the subjective perception of its intensity. In addition, various types of pain have been described in PD, mainly neuropathic or nociceptive. The presence of pain symptoms is often not taken into account in the recommendations for treatment, leaving their management at the discretion of only doctors. Studies focusing on pain frequency in such disorders suggest a high prevalence of pain in selected populations from 40% to 86% in Parkinson’s disease (PD). The methods of pain assessment vary between studies so the type of pain has been rarely reported. However, a prevalent nonneuropathic origin of pain emerged for PD. The electrophysiological investigations on 8 rats Albino lines (230±30g.) has been conducted: intacts (5 animals) and on the rotenone model of Parkinson’s disease (PD) (3 animals) has been conducted. The extracellular recording of impulse activity 229 single neurons of ventral-posterolateral nucleus (nVPL) of thalamus on high frequency stimulation of second somatosensory cortex of the brain has been produced. Analyses of relative degree frequency intensity of depressor and excitatory effects, on the bases of diagrams of average frequency of impulses, presented as disk graphs in mentioned conditions following changes of tetanic depressor and excitatory reactions, accompanied by posttetanic depressor and potentiation has been revealed. On the model of PD in both sequences, in comparison with norm, reduction in the number of neurons, responded by inhibitory poststimulus reactions has been revealed. The prestimulus frequency of nVPL neurons impulse activity, preceding to both inhibitory and excitatory sequences, in comparison with, dramatically increased turned out to be. The poststimulus frequency of impulse activity on the model of PD, accompanied by inhibitory and excitatory sequences also significantly increased turned out to be. A significant shift of frequency of pre- and poststimulus activity in pathology is a consequence of the development of excitotoxicity, that is fraught with apoptosis and dead. In conclusion, on the model of PD the excitotoxicity revealed in neurons of nVPL, leading to neurodegenerative defeat of these important antinociceptive structures of thalamus, with origin of resistant chronic pain. Marked indicates the need of protective conservation of inhibitory effects and reduced of excessive excitatory.

The major cause of Parkinson's disease is progressive disturbance of dopaminergic neurons of the substantia nigra, as well as their nerve endings located in the striatum. Therefore, therapy aimed at slowing the death of dopaminergic neurons can be effective. In recent decades, various types of neuroprotective agents have been successfully used in the treatment of neurodegenerative diseases, after which the restoration of structural disfunctions of the CNS is accelerated. In the present study, we used bacterial melanin, the therapeutic effect of which is due to the improvement of the trophic effects of the brain tissue, inhibition of the inflammatory process and gliosis. The comparative study of morphological and functional state of the substantia nigra pars compacta in a rotenone model of Parkinson's disease and combined with introduction of bacterial melanin was carried out. For morphological and histochemical study, the method of detecting the activity of Ca2 + - dependent acid phosphatase was used. The analysis of the data obtained showed that during rotenone intoxication, neuronal death and substantia nigra depigmentation are observed, as well as sharp morphological changes in intracellular structures occur, which indicates gross metabolic and morphological disorders. With the introduction of bacterial melanin, there is a tendency to preserve the normal morphological picture of the neurons of the substantia nigra pars compacta, in comparison with the Parkinson's disease model.  Thus, bacterial melanin acts as a neuroprotective agent and has a supportive role in Parkinson's disease.  Keywords:  bacterial melanin, Parkinson's Disease, substantia nigra