MicroRNAs are small noncoding RNAs, which regulate the expression of protein coding transcripts through mRNA degradation or translational inhibition. Numerous reports have highlighted the role of miRNAs in regulating cell death pathways including the expression of genes involved in the induction of apoptosis. Tumor necrosis factor alpha (TNF-α) is a proinflammatory cytokine which can send pro-death signals through its receptor TNFR1. Diverse adaptor molecules including DENN/MADD adaptor protein have been shown to modulate TNF-α pro-death signaling via recruitment of MAP kinases to TNFR1 and activation of pro-survival NFκB signaling. Herein, we investigated the role of microRNA-181 (miR-181) in regulating DENN/MADD expression levels and its subsequent effects on TNF-α-induced cell death. Using bioinformatics analyses followed by luciferase reporter assays we showed that miR-181 interacts with the 3’ UTR of DENN/MADD transcripts. miR-181 overexpression also led to decreased endogenous DENN/MADD mRNA levels in L929 murine fibroblasts. Flow cytometric analysis of miR-181 transfected cells showed this miRNA accentuates mitochondrial membrane potential loss caused by TNF-α. These findings were associated with enhanced apoptosis of L929 cells following TNF-α treatment. Overall, these data point to the potential role of miR-181 in regulating TNF-α pro-death signaling, which could be of importance from pathogenesis and therapeutic perspectives in inflammatory disorders associated with tissue degeneration and cell death.

Metals have always proved their nature as integral parts of the Earth's crus t, water, air and various ecosys tems. Rare metals are commonly used as enzyme cofactors and act to regulate the cell functions. The accumulation of metals in the brain indicates the important role of these subs tances in the nervous sys tem. The lack of these metals is associated with a variety of neurological diseases. On the other hand, enhancement of metal levels may lead to various harmful intracellular events, including oxidative s tress, mitochondrial dysfunction, DNA fragmentation, protein falsity, endoplasmic endothelial s tress, dis turbance in autophagy and induction of apoptosis. To date, adverse effects of metal imbalances with multiple human diseases, such as Alzheimer's disease, amyotrophic lateral sclerosis, autism spectrum disorders, Guillen-Barre disease, Persian Gulf War syndrome, Huntington's disease, multiple sclerosis, Parkinson's disease, and Wilson's disease, have been reported. The role of some of these metal ions, especially in brain function, is important, which led to the introduction of the term metalloneurochemis try to describe the s tudy of metallic ions in the nervous sys tem at the molecular level. Conclusion: Various metals play an important role in the regulation of multiple vital processes of neurons. Deficiency or elevated levels of any of these metals have harmful effects on the human nervous sys tem, which may contribute to different neurodegenerative diseases.

Long non-coding RNAs (lncRNAs) are regulatory molecules that set many vital processes in the cell. These regulatory RNAs, as an important component of the regulatory networks of genes and the expression of key genes involved in setting development, play an important role in neurological diseases of the central nervous system (CNS). The purpose of this study was to evaluate the regulatory functions of lncRNAs in the evolution of the CNS and an overview of their roles in the biology of neuropsychiatric diseases. More than half of all lncRNAs expressed in CNS cells and their regulated expression in the evolution and function of the nervous system are important. lncRNAs are involved in the development of different parts of the brain, specificity and differentiation of oligodendrocytes category, and terminal myelination. In addition, they have a role in regulation of vital functions, such as maintaining neural stem cells, neurogenesis and glyogenesis, homeostasis, and synaptic connections. lncRNAs are associated with the biological processes in the brain, such as the development of the hippocampus and aging. Conclusion: This review has shown that how lncRNA regulate vital processes in neurons in order to have a better understanding on the mechanisms of neurological diseases by RNA interference. Understanding the role of the regulatory RNAs interference and its impact on the biology of CNS can helpful in the field of prognosis, prediction of response to treatment, and pathological staging. Furthermore, it can be inhibited or controlled as novel therapeutic targets.

Ecstasy is a strong hallucinogenic drug, which is widely used as a street drug. It can improve mood and social relationships in the short term. Studies in humans and animals have shown that ecstasy can cause toxic effects on the nervous system. Although many research has been done on ecstasy but its mechanism of action is still not fully understood. Ecstasy is capable to inhibit serotonin in axon terminals of the brain in rats and mice. It destroyed neurons in the hippocampus, basal ganglia, insula, and parietal cortex. Heat gain, high blood pressure, arrhythmia, liver dysfunction, seizures, memory loss as well as cognitive and mood disorders are among toxic effects of this drug. There are some reports of its toxic effects on the nervous system. Evidence suggest that it can cause resistant psychotic disorders and depression in some consumer. Investigations have shown that the major cause of complications of this drug is reduction of serotonergic system activities. Frequent use of ecstasy (or its addiction) can cause the loss and degradation of the serotonergic neurons. Conclusion: Use of ecstasy is increasing and prevention of its damage to nervous system should be considered. Administration of neuroprotective substances may prevent these complications.