American journal of neurodegenerative disease最新文献

{"title":"One case with dexmedetomidine-induced stuporous state in epileptic patient undergoing abdominal surgery.","authors":"Dong-Ji Han,&nbsp;Zhi-Gang He,&nbsp;Zhi-Qiang Zhou,&nbsp;Li Feng,&nbsp;Cheng Liu,&nbsp;Yan Xiang,&nbsp;Hong-Bing Xiang","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>A 56-year-old epileptic patient underwent right hemicolectomy and cholecystectomy surgery under general endotracheal anesthesia. Anesthesia was maintained with sevoflurane, and sufentanil, rocuronium, and dexmedetomidine infusions. After the operation and confirmation of neuromuscular recovery, the patient woke from anesthesia within 15 min and successfully extubated. After the vital signs of patient were stable, the patient was transported to post anesthesia care unit (PACU). 6 h after the surgery, he fell into a stuporous state for lasting 14 h and EEG showed no epileptiform discharges. Stupor did re-occur in 2 days after operation. 36 hours after operation, all signs of the stuporous state resolved spontaneously. Apparent dexmedetomidine-induced stuporous state has not been reported in the human literature.</p>","PeriodicalId":72170,"journal":{"name":"American journal of neurodegenerative disease","volume":"6 3","pages":"26-31"},"PeriodicalIF":0.0,"publicationDate":"2017-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5545215/pdf/ajnd0006-0026.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35320040","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Can levodopa prevent cognitive decline in patients with Parkinson's disease?","authors":"Masahiro Ikeda,&nbsp;Hiroshi Kataoka,&nbsp;Satoshi Ueno","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Cognitive impairment in Parkinson's disease (PD) will become more important since the number of elderly patients with PD is increasing. We prospectively studied non-demented patients with PD over the course of 3 years to identify factors associated with PD that contribute to a decline in cognitive function. From among 100 consecutive patients, we registered 79 patients with PD. A total of 55 patients completed the study during 3 years and were divided to two groups: patients with a decline in cognitive function and those without a decline in cognitive function after 3 years. Seventeen independent variables were evaluated with the use of logistic regression models. The increase in the daily levodopa dose was related to a decline in cognitive function on univariate logistic regression analysis (OR = 0.279, p = 0.024, 95% CI = 0.092-0.848). Other variables were not related to a decline in cognitive function. The increase in the daily dose of levodopa was greater in patients without a decline in cognitive function than those with a decline in cognitive function; on the other hand, the cognitive function unchanged. Our results suggest that the treatment with levodopa might prevent a decline in cognitive function in PD.</p>","PeriodicalId":72170,"journal":{"name":"American journal of neurodegenerative disease","volume":"6 2","pages":"9-14"},"PeriodicalIF":0.0,"publicationDate":"2017-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5498848/pdf/ajnd0006-0009.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35157595","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Altered mechanisms of protein synthesis in frontal cortex in Alzheimer disease and a mouse model.","authors":"Paula Garcia-Esparcia,&nbsp;Georgios Sideris-Lampretsas,&nbsp;Karina Hernandez-Ortega,&nbsp;Oriol Grau-Rivera,&nbsp;Theodoros Sklaviadis,&nbsp;Ellen Gelpi,&nbsp;Isidro Ferrer","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Expression of the nucleolar chaperones nucleolin (<i>NCL</i>) and nucleophosmin (<i>NPM1</i>), upstream binding transcription factor (<i>UBTF</i>), rRNA18S, rRNA28S, and several genes encoding ribosomal proteins (RPs) is decreased in frontal cortex area 8 at advanced stages of Alzheimer's disease (AD). This is accompanied by reduced protein levels of elongation factors eEF1A and eEF2. Changes are more marked in AD cases with rapid course (rpAD), as initiation factor eIF3η is significantly down-regulated and several RP genes up-regulated in rpAD when compared with typical AD. These changes contrast with those seen in APP/PS1 transgenic mice used as a model of AD-like β-amyloidopathy; <i>Ncl</i> mRNA, rRNA18S, rRNA28S and seven out of fifteen assessed RP genes are up-regulated in APP/PS1 mice aged 20 months; only eEF2 protein levels are reduced in transgenic mice. Our findings show marked altered expression of molecules linked to the protein synthesis machinery from the nucleolus to the ribosome in frontal cortex at terminal stages of AD which differs from that seen in APP/PS1 transgenic mice, thus further suggesting that molecular signals in mouse models do not apply to real human disease counterparts.</p>","PeriodicalId":72170,"journal":{"name":"American journal of neurodegenerative disease","volume":"6 2","pages":"15-25"},"PeriodicalIF":0.0,"publicationDate":"2017-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5498849/pdf/ajnd0006-0015.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35157596","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Etiology and treatment of amyotrophic lateral sclerosis.","authors":"Hernando Rafael,&nbsp;Juan Oscar David,&nbsp;Antonio Santiago Vilca","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Background: </strong>To date all researchers conclude that the etiology of Amyotrophic lateral sclerosis (ALS) is not known. On the contrary, since August 2009, we believe that disease is of ischemic origin in the anterior surface of the medulla oblongata.</p><p><strong>Material and method: </strong>We present our surgical experience into 45 patients with ALS (bulbar form in 36 cases and spinal form in 9). Preoperative MRI scans revealed microinfarcts in the medulla oblongata and/or cervical cord. During surgery we found: 1) poor quality of omentum in most cases; 2) degenerative changes in the cervical spine; 3) anatomical anomalies at the V4 segments of the vertebral arteries; 4) moderate to severe atherosclerosis at both V4 segments; 5) unilateral absence or stenosis in the anterior-ventral spinal arteries (AVSAs). All patients received omentum on the anterior, lateral and posterior surface of the medulla oblongata, and in 9 cases, an additional segment at the C5-C6 level.</p><p><strong>Results: </strong>Neurological improvement was better during the first days or weeks after surgery than in the following months or years, in all patients. However, 13 patients suffered neurological impairment in about 4 months later, due to greater deterioration of the cervical spine, by contrast, 7 patients with mild ALS have experienced neurological improvement by 80 to 100% during a follow-up of 4 and 6 years.</p><p><strong>Conclusions: </strong>These results confirm that ALS is of ischemic origin in the intraparenchymal territory of the AVSAs and/or in anterior spinal artery caused by atherosclerosis and associated to anatomical variants in the V4 segments of the vertebral arteries. Because in contrast to this, its revascularization by means of omentum can cure (mild degree) or improve this disease.</p>","PeriodicalId":72170,"journal":{"name":"American journal of neurodegenerative disease","volume":"6 1","pages":"1-8"},"PeriodicalIF":0.0,"publicationDate":"2017-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5435608/pdf/ajnd0006-0001.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35018541","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fundamental role of pan-inflammation and oxidative-nitrosative pathways in neuropathogenesis of Alzheimer's disease [Retraction].","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>[This retracts the article on p. 1 in vol. 5, PMID: 27073740.]. </p>","PeriodicalId":72170,"journal":{"name":"American journal of neurodegenerative disease","volume":"5 3","pages":"152"},"PeriodicalIF":0.0,"publicationDate":"2016-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4965615/pdf/ajnd0005-0152.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34743491","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Omental transplantation in a patient with mild ALS.","authors":"Hernando Rafael","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>To demonstrate that amyotrophic lateral sclerosis (ALS) is not a neurodegenerative disease. The patient, a 33-year-old man began with symptoms of the bulbar form of ALS, characterized by burning pain in both feet during two months and then, he presented right crural monoparesis, fasciculations, slight dysarthria and he walked with help of orthopedic devices. A preoperative MRI scans showed atherosclerosis at the V4 segment of the left vertebral artery. On May 2012, he received an omental transplantation on the anterior, left lateral and posterior surface of the medulla oblongata. About 48 hours after surgery, the dysarthria disappeared and the voluntary movement of the right foot improved. Three days later, he walked without aid of orthopedic device. At present, four years after operation he present complete reversal of symptoms. In conclusión, this patient confirms that bulbar ALS is of ischemic origin and therefore, mild ALS can be cured. </p>","PeriodicalId":72170,"journal":{"name":"American journal of neurodegenerative disease","volume":"5 3","pages":"153-7"},"PeriodicalIF":0.0,"publicationDate":"2016-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4965616/pdf/ajnd0005-0153.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34743492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fundamental role of pan-inflammation and oxidative-nitrosative pathways in neuropathogenesis of Alzheimer's disease in focal cerebral ischemic rats.","authors":"Mak Adam Daulatzai","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a chronic progressive neurodegenerative condition of the brain, and it is the most common cause of dementia. Several neurobiological etiologies of AD are described in the literature. These include vascular, infectious, toxic, nutritional, metabolic, and inflammatory. However, these heterogeneous etiologies have a common denominator - viz. Inflammation and oxidative stress. Lipopolysaccharide (LPS) elevates the synthesis of proinflammatory cytokines and chemokines; chronically, together they trigger various pathological responses in the periphery and the CNS including dysfunctional memory consolidation and memory decline. Aging - the main risk factor for AD is inherently associated with inflammation. There are several age-related comorbidities that are also associated with inflammation and oxidative stress. Such co-prevailing aggravating factors, therefore, persist against a background of underlying aging-related pathology. They may converge, and their synergistic propagation may modify the disease course. A critical balance exists between homeostasis/repair and inflammatory factors; chronic, unrelenting inflammatory milieu succeeds in promoting a neuroinflammatory and neurodegenerative outcome. Extensive evidence is available that CNS inflammation is associated with neurodegeneration. LPS, proinflammatory cytokines, several mediators secreted by microglia, and oxidative-nitrosative stress in concert play a pivotal role in triggering neuroinflammatory processes and neurodegeneration. The persistent uncontrolled activity of the above factors can potentiate cognitive decline in tandem enhancing vulnerability to AD. Despite significant progress during the past twenty years, the prevention and treatment of AD have been tantalizingly elusive. Current studies strongly suggest that amelioration/prevention of the deleterious effects of inflammation may prove beneficial in preventing AD onset and retarding cognitive dysfunction in aging and AD. A concerted multi-focal therapeutic effort around the inflammation-oxidative-nitrosative stress paradigm may be crucial in preventing and treating AD. This paper informs on such relevant polypharmacy approach. </p>","PeriodicalId":72170,"journal":{"name":"American journal of neurodegenerative disease","volume":"5 2","pages":"102-30"},"PeriodicalIF":0.0,"publicationDate":"2016-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4913220/pdf/ajnd0005-0102.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34668336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ganoderma Lucidum polysaccharides protect against MPP(+) and rotenone-induced apoptosis in primary dopaminergic cell cultures through inhibiting oxidative stress.","authors":"Shan-Shan Guo,&nbsp;Xiao-Lan Cui,&nbsp;Wolf-Dieter Rausch","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Oxidative stress plays a pivotal role in the progressive neurodegeneration in Parkinson's disease (PD) which is responsible for disabling motor abnormalities in more than 6.5 million people worldwide. Polysaccharides are the main active constituents from Ganoderma lucidum which is characterized with anti-oxidant, antitumor and immunostimulant properties. In the present study, primary dopaminergic cell cultures prepared from embryonic mouse mesencephala were used to investigate the neuroprotective effects and the potential mechanisms of Ganoderma lucidum polysaccharides (GLP) on the degeneration of dopaminergic neurons induced by the neurotoxins methyl-4-phenylpyridine (MPP(+)) and rotenone. Results revealed that GLP can protect dopamine neurons against MPP(+) and rotenone at the concentrations of 100, 50 and 25 μg/ml in primary mesencephalic cultures in a dose-dependent manner. Interestingly, either with or without neurotoxin treatment, GLP treatment elevated the survival of THir neurons, and increased the length of neurites of dopaminergic neurons. The Trolox equivalent anti-oxidant capacity (TEAC) of GLP was determined to be 199.53 μmol Trolox/g extract, and the decrease of mitochondrial complex I activity induced by MPP(+) and rotenone was elevated by GLP treatment (100, 50, 25 and 12.5 μg/ml) in a dose dependent manner. Furthermore, GLP dramatically decreased the relative number of apoptotic cells and increased the declining mitochondrial membrane potential (ΔΨm) induced by MPP(+) and rotenone in a dose-dependent manner. In addition, GLP treatment reduced the ROS formation induced by MPP(+) and rotenone at the concentrations of 100, 50 and 25 μg/ml in a dose-dependent manner. Our study indicates that GLP possesses neuroprotective properties against MPP(+) and rotenone neurotoxicity through suppressing oxidative stress in primary mesencephalic dopaminergic cell culture owning to its antioxidant activities. </p>","PeriodicalId":72170,"journal":{"name":"American journal of neurodegenerative disease","volume":"5 2","pages":"131-44"},"PeriodicalIF":0.0,"publicationDate":"2016-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4913221/pdf/ajnd0005-0131.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34604493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of fish oil on glutathione redox system in multiple sclerosis.","authors":"Tania E Sorto-Gomez,&nbsp;Genaro G Ortiz,&nbsp;Fermín P Pacheco-Moises,&nbsp;Erandis D Torres-Sanchez,&nbsp;Viridiana Ramirez-Ramirez,&nbsp;Miguel A Macias-Islas,&nbsp;Alfredo Celis de la Rosa,&nbsp;Irma E Velázquez-Brizuela","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Unlabelled: </strong>Multiple sclerosis (MS) is a chronic, inflammatory and autoimmune disease of the central nervous system. Dysregulation of glutathione homeostasis and alterations in glutathione-dependent enzyme activities are implicated in the induction and progression of MS. Evidence suggests that Omega-3 polyunsaturated fatty acids (PUFAs) have anti-inflammatory, antioxidant and neuroprotective effects. The aim of the present work was to evaluate the effect of fish oil on the activity of glutathione reductase (GR), content of reduced and oxidized glutathione, and GSH/GSSG ratio in MS. 50 patients with relapsing-remitting MS were enrolled. The experimental group received orally 4 g/day of fish oil for 12 months. Fish oil supplementation resulted in a significant increase in n-3 fatty acids and a decrease n-6 fatty acids. No differences in glutathione reductase activity, content of reduced and oxidized glutathione, and GSH/GSSG ratio were found.</p><p><strong>Conclusion: </strong>Glutathione reductase activity was not significantly different between the groups; however, fish oil supplementation resulted in smaller increase in GR compared with control group, suggesting a possible effect on antioxidant defence mechanisms.</p>","PeriodicalId":72170,"journal":{"name":"American journal of neurodegenerative disease","volume":"5 2","pages":"145-51"},"PeriodicalIF":0.0,"publicationDate":"2016-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4913222/pdf/ajnd0005-0145.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34604494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ebi, a Drosophila homologue of TBL1, regulates the balance between cellular defense responses and neuronal survival.","authors":"Young-Mi Lim,&nbsp;Leo Tsuda","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Transducin β-like 1 (TBL1), a transcriptional co-repressor complex, is a causative factor for late-onset hearing impairments. Transcriptional co-repressor complexes play pivotal roles in gene expression by making a complex with divergent transcription factors. However, it remained to be clarified how co-repressor complex regulates cellular survival. We herein demonstrated that ebi, a Drosophila homologue of TBL1, suppressed photoreceptor cell degeneration in the presence of excessive innate immune signaling. We also showed that the balance between NF-κB and AP-1 is a key component of cellular survival under stress conditions. Given that Ebi plays an important role in innate immune responses by regulating NF-κB activity and inhibition of apoptosis induced by associating with AP-1, it may be involved in the regulation of photoreceptor cell survival by modulating cross-talk between NF-κB and AP-1. </p>","PeriodicalId":72170,"journal":{"name":"American journal of neurodegenerative disease","volume":"5 1","pages":"62-8"},"PeriodicalIF":0.0,"publicationDate":"2016-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4788732/pdf/ajnd0005-0062.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34311625","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}