Search

Cognitive dysfunction is a state of losing or having difficulties in remembering, learning, focusing, or making decisions that impact individual healthy life. Small single-stranded and nonprotein coding RNAs, microRNAs (miRNAs) participate actively in regulatory processes, incorporate cognitive signaling pathways, and intensely affect cognitive evolution. miRNAs exert their modification activities through translational or transcriptional processes. Reportedly, cognitive impairment and dementia are rising, especially in developing countries. Herein we provided a brief review of original studies addressing miRNA changes in the most common neurological diseases with a focus on dementia and Alzheimer's disease. It must be noted that an increase in the level of certain miRNAs but a decrease in other ones deteriorate cognitive performance. The current review revealed that induction of miR-214-3p, miR-302, miR-21, miR- 200b/c, miR-207, miR-132, miR-188-3p and 5p, and miR-873 improved cognitive impairment in various cognitive tasks. On the other hand, intentionally lowering the level of miR-34a, miR-124, miR-574, and miR-191a enhanced cognitive function and memory. Synaptic dysfunction is a core cause of cognitive dysfunction; miRNA-34, miRNA-34-c, miRNA-124, miRNA-188-5p, miRNA-210-5p, miRNA-335-3p, and miRNA-134 strongly influence synaptic-related mechanisms. The downregulation of miRNA-132 aggregates both amyloid and tau in tauopathy. Concerning the massive burden of neurological diseases worldwide, the future challenge is the translation of animal model knowledge into the detection of pathophysiological stages of neurocognitive disorders and designing efficient therapeutic strategies. While the delivery procedure of agomir or antagomir miRNAs into the brain is invasive and only applied in animal studies, finding a safe and specific delivery route is a priority.

Introduction: The pharmacological suppression of luteinising hormone or human chorionic gonadotropin (hCG) can reduce Aβ plaques in the brains of rats and mice, but the effects of hCG on the phosphorylated tau protein level in the hippocampus have not been studied. Therefore, we investigated the effects of hCG on the phosphorylated tau protein level and its effect on hCG receptor-immunoreactive neuron density in the hippocampus of Alzheimer's disease (AD) model rats (streptozotocin STZ injected intracerebroventricularly). Material and methods: The rats were administered hCG (50, 100, and 200 IU/200 µl saline, intraperitoneally) or vehicle once/day for three days after injection of STZ. The passive avoidance memory test was performed 6 hours after the last hCG injection. The phosphorylated tau protein level in the hippocampus was measured by ELISA, and hCG receptor-immunoreactive neurons were shown by immunohistochemical technique in areas of hippocampus. Results: Treatment with hCG attenuated memory deficiencies and reduced the level of phosphorylated tau protein in the hippocampus. hCG also improved the density of hCG receptor-immunoreactive neurons. The high dose of hCG hormone (200 IU/200 µl saline) seemed to have a significant effect on passive avoidance memory, phosphorylated tau protein concentration, and accumulation of hCG receptor-immunoreactive neurons in Alzheimeric rats' hippocampus. Conclusions: In conclusion, hCG can provide protection against memory deficits induced by STZ and it can inhibit accumulation of tau hyperphosphorylation in the hippocampus. Furthermore, hCG can increase the hCG receptor-ir neurons number in the rats hippocampus after ICV injection of STZ. © 2018 Termedia Publishing House Ltd. All Rights Reserved.

Age-associated changes in the levels of luteinizing hormone and human chorionic gonadotropin (hCG) are potential risk factors for Alzheimer's disease (AD); hCG concentration is related to the incidence of AD. The highest density of hCG receptors is in zones of the brain that are vulnerable to AD and streptozotocin (STZ) can decrease the density of this receptor. We investigated the effects of different doses of hCG on hCG receptor density in the prefrontal cortex and cerebellum in a rat model of STZ-induced AD. AD was induced by intracerebroventricular injection of 3 mg/kg STZ. The resulting AD rats were treated for 3 days with 50, 100 or 200 IU/200 μl hCG, or with saline as a control. Sections of prefrontal cortex and cerebellum were stained immunohistochemically and hCG receptor-immunoreactive (ir) neurons were counted. STZ injected into the lateral ventricles of rat brains reduced the density of hCG receptor-ir neurons in the prefrontal cortex and cerebellum. hCG administration resulted in a significant dose-dependent increase in the number of hCG receptor-ir neurons in the prefrontal cortex and cerebellum. The maximum increase in the number of receptors occurred following the 200 IU dose of hCG. Administration of hCG ameliorated the lowered density of hCG receptor-ir neurons in the cerebellum and prefrontal cortex in STZ-induced AD rats.