Summary
Alzheimer’s disease (AD) is an age-related neurodegenerative disorder clinically characterized by memory impairment, disorientation, cognitive deficits, and behavioral disturbances. The neuropathological features are amyloid plaques containing aggregated amyloid-beta (Aβ) peptide, neurofibrillary tangles composed of the hyperphosphorylated form of the microtubule protein tau (HP-tau), and loss of neurons and synapses in the brain.
There are no effective strategies for the prevention or treatment of the disease, leading to an increased need for AD biomarkers to improve early detection, accurate diagnosis, and accelerate drug development in this field. Recently, increasing attention has been dedicated to neuropeptides in searching for new drug targets in the treatment of nervous system disorders. Available data suggest that many neuropeptides may be associated with the pathophysiology and potential therapy of AD because of their wide distribution in brain areas responsible for learning and memory processes and their predominately neuroprotective actions. This short review aimed to briefly describe the neuropathology of AD and summarize the data related to one of its recently proposed biomarker - kyotorphin (KTP) neuropeptide. Our previous experiments showed moderate and selective protective effects of KTP against the late consequences of the intracerebroventricular streptozotocin-induced AD model.
Introduction: The endogenous dipeptide L-tyrosine-L-arginine (kyotorphin, KTP) is found in brain structures related to the processing of information for nociception, the control of emotions, and memory formation. Besides the antinociceptive effect of KTP, it has a mild protective activity against the deleterious influence of the brain hypoperfusion and streptozotocin on the behavior and memory.
Aim: We aimed to study the effects of the intracerebroventricular injection of effective antinociceptive doses of KTP on the motivational behavior, memory, and blood and hippocampal levels of the carbonylated proteins in healthy male adult Wistar rats.
Materials and methods: We used a paw-pressure test for assessment of acute nociception, an open field test for assessment of exploration and habituation to a new environment, elevated plus maze test for the evaluation of anxiety-like behavior, and novel object recognition test for working memory. Carbonylated protein assay was used for the assessment of the oxidative impairment of the proteins. The results were analyzed by ANOVA.
Results: The present data showed that all single doses of KTP exerted an antinociceptive effect, but this effect was not observed after chronic administration. Only the highest dose of 100 µg was able to induce anxiolytic and motor inhibiting effects. None of the doses used showed effects on the recognition memory or the level of the carbonylated protein.
Conclusion: Our results showed that KTP exerted its antinociceptive effect without affecting negatively the blood and brain carbonylated protein or basic behavioral parameters related to the exploration, motivation, and memory formation in healthy rats.
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