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Background@#and Purpose Cognitive impairment (CI) is a common symptom of multiple sclerosis (MS). Although demographic and clinical factors contribute to MS-dependent CI, previous findings have been inconsistent. This study aimed to identify the cognitive domains that are impaired in MS patients, and to determine the impacts of the Expanded Disability Status Scale (EDSS) score and other clinical and demographic factors on them domains. @*Methods@#This study enrolled 115 MS patients. Cognitive performance was assessed using the Minimal Assessment of Cognitive Function in Multiple Sclerosis (MACFIMS) battery. CI severity was assessed based on the number of impaired tasks in the MACFIMS battery, with impairment in two or more tasks defined as CI cases. Correlation analysis was used to determine whether factors including current age, age at disease onset, EDSS score, disease duration, relapse rate, and education level affect the severity of CI. @*Results@#The scores on the Paced Auditory Serial Addition Test and Delis-Kaplan Executive Function System were the most and least affected, respectively. EDSS score (r=0.438, p<0.001), current age (r=0.393, p<0.001), and disease duration (r=0.486, p<0.001) were positively correlated with CI severity, whereas education level (r=-0.527, p<0.001) had a negative correlation with CI severity, and age at disease onset and relapse rate were not correlated with CI severity (r=0.150 and p=0.107, and r=0.052 and p=0.530, respectively). However, all variables (except EDSS score) significantly predicted CI severity in a multiple regression model (p<0.001, r=0.668). @*Conclusions@#Information processing speed and working memory were the most commonly affected cognitive domains in the present MS patients. CI severity had strong positive correlations with current age, EDSS score, and disease duration, and a negative correlation with education level. The relapse rate and age at disease onset were not correlated with CI severity.
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Purpose@#Neurogenic bladder dysfunction (NGB) has an impact on the quality of life, which made it an important research subject in preclinical studies. The present review investigates the effect of stem cell (SC) therapy on bladder functional recovery after the onset of spinal cord injury (SCI), multiple sclerosis (MS), Parkinson disease (PD), and stroke in rodent models. @*Methods@#All experiments evaluated the regenerative potential of SC on the management of NGB in rodent models up to June 2019, were included. From 1,189 relevant publications, 20 studies met our inclusion criteria of which 15 were conducted on SCI, 2 on PD, 2 on stroke, and 1 on MS in the rodent models. We conducted a meta-analysis on SCI experiments and for other neurological diseases, detailed urodynamic findings were reported. @*Results@#The common SC sources used for therapeutical purposes were neural progenitor cells, bone marrow mesenchymal SCs, human amniotic fluid SCs, and human umbilical cord blood SCs. There was a significant improvement of micturition pressure in both contusion and transaction SCI models 4 and 8 weeks post-SC transplantation. Residual urine volume, micturition volume, and bladder capacity were improved 28 days after SC transplantation only in the transaction model of SCI. Nonvoiding contraction recovered only in 56 days post-cell transplantation in the contusion model. @*Conclusions@#Partial bladder recovery has been evident after SC therapy in SCI models. Due to limitations in the number of studies in other neurological diseases, additional studies are necessary to confirm the detailed mechanism for bladder recovery.
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Background: Ghrelin is a peptide with attenuating effect on inflammatory pain. Both anti- and pro-inflammatory mediators have a role in the nociception and development of pain and hyperalgesia. IL-10 and TGF-beta are anti-inflammatory cytokines and inhibit the expression of pro-inflammatory cytokines related to peripheral and central inflammatory pain. In this study, the effects of i.p. injection of ghrelin on the early and the late phases of pain, as well as serum levels of IL-10 and TGF-beta, as anti-inflammatory cytokines, were investigated in formalin-induced pain in male rats
Methods: Adult male Wistar rats [n=48] were randomly divided into six groups: control, formalin+saline, ghrelin [40, 80, and 160 microg/kg], and morphine. Ghrelin was administered i.p. 30 min before inducing pain by formalin. Pain induced by intraplantar [i.pl.] injection of 50 microl formalin 5%, and pain behavior was studied for 60 min. Serum IL-10 and TGF-beta levels were assessed by ELISA method
Results: The findings of the present study showed that ghrelin with high doses [80 and 160 microg/kg] significantly reduced pain intensity in both the early and the late phases of pain. The serum levels of cytokines, IL-10, and TGF-beta1 showed a significant elevation with ghrelin at dose of 160 microg/kg
Conclusion: Ghrelin is effective in reducing the intensity of both the early and the late phases of inflammatory pain. It seems that ghrelin exerts its analgesic effects in part by increasing the serum levels of anti-inflammatory cytokines
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Objective: This study was designed to evaluate whether chronic Rosa canina [RC] extract administration could improve recognition memory and depressive-like behavior in diabetic mice
Materials and Methods: Seventy-five male albino mice [25-30 g] were randomly divided into 5 groups [15 in each group]
A single intraperitoneal injection of 200 nng/ kg streptozotocin [STZ] was administered to the mice to induce diabetes
The control group received normal saline, and the diabetic groups received normal saline or 50, 250, and 500 mg/kg of RC extract for 28 days
The mice were weighed each week
Recognition memory and depressive-like behavior were assessed using forced swimming and novel object recognition [NOR] tests, respectively. Malondi-aldehyde [MDA] levels and total antioxidant capacity [TAG]were measured in the mouse brain homogenate to evaluate oxidative stress. Statistical analysis was conducted using SPSS, version 22
Results: The groups receiving 250 or 500 mg/kg RC had significantly lower immobility time [159.4 +/- 4.7 and 150.1 +/- 3.1 s] compared to the sham control group [192.1 +/- 7.8 s] in the forced swimming test, and a higher discrimination index [0.39 +/- 0.02 and 0.48 +/- 0.03] was seen in diabetic animals in the NOR task compared to the sham control group [0.2 +/- 0.01]
Also, the groups receiving treatment with RC [250 and 500 mg/kg] had significantly higher TAG [0.92 +/- 0.04 and 0.96 +/- 0.05 mmol/L] and lower MDA [0.76 +/- 0.02 and 0.67 +/- 0.03 nmol/mg protein] levels in the brains in comparison to the model group. In the 3rd and 4th weeks of study, the RC-treated mice [250 and 500 mg/kg] gained more weight [31.2 +/- 0.3 and 32.4 +/- 0.3 g, and 31.3 +/- 0.2 and 33.7 +/- 0.3 g, respectively] than the diabetic group [30 +/- 0.2 and 29.6 +/- 0.3 g]
Conc/us/on:This study showed that RG attenuated impairment of recognition memory and depressive-like behavior probably through modulation of oxidative stress in an STZ model of diabetes in mouse brains
Subject(s)
Animals, Laboratory , Male , Oxidative Stress , Depressive Disorder/drug therapy , Recognition, Psychology , Memory Disorders/drug therapy , Diabetes Mellitus, Experimental , MiceABSTRACT
Alzheimer's disease [AD] is the most prevalent form of dementia which affects people older than 60 years of age. In AD, the dysregulation of the amyloid-beta [Abeta] level leads to the appearance of senile plaques which contain Abeta depositions. Abeta is a complex biological molecule which interacts with many types of receptors and/or forms insoluble assemblies and, eventually, its nonphysiological depositions alternate with the normal neuronal conditions. In this situation, AD signs appear and the patients experience marked cognitional disabilities. In general, intellect, social skills, personality, and memory are influenced by this disease and, in the long run, it leads to a reduction in quality of life and life expectancy. Due to the pivotal role of Abeta in the pathobiology of AD, a great deal of effort has been made to reveal its exact role in neuronal dysfunctions and to finding efficacious therapeutic strategies against its adverse neuronal outcomes. Hence, the determination of its different molecular assemblies and the mechanisms underlying its pathological effects are of interest. In the present paper, some of the well-established structural forms of Abeta, its interactions with various receptors and possible molecular and cellular mechanisms underlying its neurotoxicity are discussed. In addition, several Abeta-based rodent models of AD are reviewed