Treadmill exercise attenuates 3,4-methylenedioxymethamphetamine-induced memory impairment through a decrease apoptosis in male rat hippocampus.

3,4-methylenedioxymethamphetamine (MDMA) leads to apoptosis in the hippocampus with consequent induction of learning and memory impairment. In this study, we have investigated the effects of treadmill exercise on memory in relation to apoptosis and oxidative stress in the hippocampi of MDMA-treated rats. Male Wistar rats received multiple intraperitoneal (IP) injections of MDMA (10 mg/kg) and exercised for one month on a treadmill (simultaneously or asynchronously with MDMA). We assessed memory function with the Morris water maze (MWM) test. Lipid peroxidation (LPO) and expression of caspase 3, Bax, and Bcl-2 were examined by the thiobarbituric acid assay (TBA) and western blot, respectively. Our results showed that asynchronous treadmill exercise could significantly improve MDMA-induced memory impairment in the MWM test. Caspase 3 expression decreased in the exercise group compared to the MDMA group. Although MDMA treatment caused an increase in the Bax/Bcl-2 ratio, the treadmill exercise reduced this ratio. Simultaneous exercise caused a reduction in lipid peroxidation in the hippocampus. This data suggests that treadmill exercise can be a useful strategy for treating memory impairment in persons with neurodegenerative disease and stimulant drug users. © 2017 Wiley Periodicals, Inc.

Erratum to: Treadmill exercise alters ecstasy- induced long- term potentiation disruption in the hippocampus of male rats.

In the original publication of the article, author name Masoumeh Asadbegi was incorrectly written as Masoumeh Asadbeigi. The authors regret the oversight.

Treadmill exercise alters ecstasy- induced long- term potentiation disruption in the hippocampus of male rats.

3, 4-methylenedioxymethamphetamine (MDMA) or ecstasy is a derivative of amphetamine that leads to long term potentiation (LTP) disruption in the hippocampal dentate gyrus (DG). Exercise has been accepted as a treatment for the improvement of neurodegenerative disease. Herein, the effects of exercise on the MDMA- induced neurotoxicity were assessed. Male Wistar rats received intraperitoneal injection of MDMA (10 mg/kg) and exercised for one month on a treadmill (Simultaneously or asynchronously with MDMA). LTP and expression of BDNF were assessed using electrophysiology and western blotting methods, respectively. MDMA attenuated the field excitatory post-synaptic potential (fEPSP) slope in comparison with the control group, whereas treadmill exercise increased this parameter when compared to MDMA group. Furthermore, BDNF expression significantly decreased in MDMA group and treadmill exercise could increase that. In conclusion, results of this study suggest that synchronous exercise is able to improve MDMA-induced LTP changes through increase of BDNF expression in the hippocampus of rats.

Expression analysis of Treg-related lncRNAs in neuromyelitis optica spectrum disorder.

Neuromyelitis Optica Spectrum Disorder (NMOSD) is an autoimmune condition affecting the central nervous system, in which various kinds of immune cells, including T and B cells, and numerous cytokines and chemokines are implicated. LncRNAs modulating the function or differentiation of regulatory T cells (Tregs) may be involved in the pathoetiology of NMO. To assess the involvement of these lncRNAs in this disease, we studied the expression levels of TH2-LCR, MAFTRR, NEST, RMRP, and FLICR in NMO patients and healthy subjects. All of the lncRNAs listed were up-regulated in NMO patients compared with healthy controls. Although the interaction of group and gender factors significantly affected the expression of NEST, RMRP, and TH2-LCR genes, we detected no effect of gender factor on the expression of the examined genes. The highest expression correlation was found between RMRP and TH2-LCR among cases with correlation coefficient 0.73. ROC curve analysis indicated that TH2-LCR, MAFTRR, RMRP, and FLICR had significant prospective diagnostic power (AUC ± SD = 0.99 ± 0.002, 0.97 ± 0.01, 0.91 ± 0.01 and 0.84 ± 0.04, respectively). Best of these genes was TH2-LCR with AUC ± SD = 0.99 ± 0.002, sensitivity= 0.97, specificity= 1, P-value= <0.0001. RMRP and TH2-LCR had a positive correlation with age and age at onset and a negative correlation with EDSS. Cumulatively, TH2-LCR, MAFTRR, RMRP, and FLICR lncRNAs, particularly TH2-LCR, could be considered as potential contributors to the pathogenesis of NMO disease.

Significant up-regulation of lncRNAs in neuromyelitis optica spectrum disorder.

Neuromyelitis optica spectrum disorder (NMOSD) is an immune-related demyelinating defect. Long non-coding RNAs (lncRNAs) might influence the pathobiology and progression of NMOSD. The current study assessed expression level of NEAT1, PANDAR, MEG3 and TUG1 lncRNAs in the peripheral blood of NMOSD patients compared with healthy individuals. All mentioned lncRNAs were shown to be over-expressed in total NMOSD cases, male NMOSD cases and female NMOSD cases compared with the matching control subgroups. MEG3 had the most robust over-expression in patients subgroups compared with normal subjects. There was no noteworthy difference in the expression of any of lncRNAs between female and male patients. MEG3 had an ideal performance in the differentiation of NMOSD cases from healthy persons (Sensitivity and specificity values = 100%). Other lncRNAs could also efficiently separate NMOSD cases from control subjects (AUC values = 0.97, 0.89 and 0.88 for PANDAR, NEAT1 and TUG1, respectively). Cumulatively, NEAT1, PANDAR, MEG3 and TUG1 lncRNAs can be considered as appropriate disease markers for NMOSD.

LncRNA signature in colorectal cancer.

Colorectal cancer (CRC) is among the most frequent cancers and is associated with high mortality particularly when being diagnosed in advanced stages. Although several environmental and intrinsic risk factors have been identified, the underlying cause of CRC is not clear in the majority of cases. Several studies especially in the recent decade have pointed to the role of epigenetic factors in this kind of cancer. Long non-coding RNAs (lncRNAs) as important contributors in the epigenetic mechanisms are involved in the initiation, progression and metastasis of CRC. Tens of oncogenic lncRNAs and a lower number of tumor suppressor lncRNAs have been recently identified to be dysregulated in CRC cells and tissues. Notably, expressions of a number of these transcripts have been dysregulated in serum samples of CRC patients, providing a non-invasive route for detection of this kind of cancer. The involvement of lncRNAs in the regulation of autophagy has provided them the ability to modulate response of CRC cells to chemotherapeutic modalities. In the current manuscript, we review the studies which evaluated the role of lncRNAs in the pathogenesis and progression of CRC to appraise their application as diagnostic/ prognostic markers.

Deferoxamine preconditioning enhances the protective effects of stem cells in streptozotocin-induced Alzheimer's disease.

AIMS: Stem cell-based therapy is one of the promising strategies in the treatment of Alzheimer's disease (AD), but the short lifespan and low homing of transplanted cells continue to be a major obstacle in this method. Preconditioning of stem cells before transplantation could increase cell therapy efficiency. Herein, we examined whether the treatment of stem cells with deferoxamine (DEF) prior to graft could enhance the neuroprotective effects of stem cells in the streptozotocin (STZ)-treated male rats. MATERIALS AND METHODS: After induction of the AD model, the rats were transplanted with DEF-preconditioned Adipose-derived mesenchymal stem cells (AMSCs) or untreated cells. Memory function, antioxidant capacity, cell density, and homing of transplanted cells were assessed using Morris water maze and shuttle box tasks as well as biochemical and histochemical methods. KEY FINDINGS: Transplantation of AMSCs caused a memory improvement when compared to the AD model. The injection of DEF-preconditioned AMSCs was more effective in improving learning and memory than the untreated cells through an increase in the antioxidant capacity. Moreover, the homing of transplanted cells was higher in the rats that received the preconditioned cells than that of the naïve cell-injected group. SIGNIFICANCE: It seems that the transplantation of DEF-treated cells may increase the efficiency of stem cells via an increase in the antioxidant capacity.

Prevalence of depression among amyotrophic lateral sclerosis (ALS) patients: A systematic review and meta-analysis

BACKGROUND: Amyotrophic lateral sclerosis (ALS) people have a high risk of severe mental disorders, like depression, which impacts their function, quality of life, and mobility. However, there are no estimates of depression based paper published. This study aimed conduct a systematic review and meta-analysis of the prevalence of depression in ALS patients around the world. METHODS: PubMed/Medline, Web of science, Scopus, Embase, and Ovid are searched to identify papers that reporting the prevalence of depression. Studies are included in random-effects meta-analyses of the prevalence of depression. Subgroup analyses are performed on the severity of depression, instruments of depression, type of studies, and study regions. RESULTS: 46 eligible studies reported prevalence of depression. The pooled prevalence of depression among ALS people was 34% (27%-41%). According to the severity of depression, mild, moderate, and severe depression were 29%, 16%, and 8%, respectively. For studies using BDI, PHQ, and HADS, the pooled prevalence of depression was 50%, 20%, and 15%, respectively. CONCLUSIONS: ALS people have a high prevalence of depression. The high prevalence of depression causes a reduction of quality of life and mobility. The study identifies a population group at high risk needing special attention in clinical practice.