{"title":"Death Receptors in the Selective Degeneration of Motoneurons in Amyotrophic Lateral Sclerosis.","authors":"Julianne Aebischer, Nathalie Bernard-Marissal, Brigitte Pettmann, Cédric Raoul","doi":"10.1155/2013/746845","DOIUrl":"https://doi.org/10.1155/2013/746845","url":null,"abstract":"<p><p>While studies on death receptors have long been restricted to immune cells, the last decade has provided a strong body of evidence for their implication in neuronal death and hence neurodegenerative disorders such as amyotrophic lateral sclerosis (ALS). ALS is a fatal paralytic disorder that primarily affects motoneurons in the brain and spinal cord. A neuroinflammatory process, associated with astrocyte and microglial activation as well as infiltration of immune cells, accompanies motoneuron degeneration and supports the contribution of non-cell-autonomous mechanisms in the disease. Hallmarks of Fas, TNFR, LT-βR, and p75(NTR) signaling have been observed in both animal models and ALS patients. This review summarizes to date knowledge of the role of death receptors in ALS and the link existing between the selective loss of motoneurons and neuroinflammation. It further suggests how this recent evidence could be included in an ultimate multiapproach to treat patients. </p>","PeriodicalId":16405,"journal":{"name":"Journal of Neurodegenerative Diseases","volume":"2013 ","pages":"746845"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/746845","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33959378","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}
Amrutha Chilumuri, Maria Ashioti, Amanda N Nercessian, Nathaniel G N Milton
{"title":"Immunolocalization of Kisspeptin Associated with Amyloid-β Deposits in the Pons of an Alzheimer's Disease Patient.","authors":"Amrutha Chilumuri, Maria Ashioti, Amanda N Nercessian, Nathaniel G N Milton","doi":"10.1155/2013/879710","DOIUrl":"https://doi.org/10.1155/2013/879710","url":null,"abstract":"<p><p>The pons region of the Alzheimer's disease (AD) brain is one of the last to show amyloid-β (Aβ) deposits and has been suggested to contain neuroprotective compounds. Kisspeptin (KP) is a hormone that activates the hypothalamic-pituitary-gonadal axis and has been suggested to be neuroprotective against Aβ toxicity. The localization of KP, plus the established endogenous neuroprotective compounds corticotropin releasing hormone (CRH) and catalase, in tissue sections from the pons region of a male AD subject has been determined in relation to Aβ deposits. Results showed Aβ deposits also stained with KP, CRH, and catalase antibodies. At high magnification the staining of deposits was either KP or catalase positive, and there was only a limited area of the deposits with KP-catalase colocalization. The CRH does not bind Aβ, whilst both KP and catalase can bind Aβ, suggesting that colocalization in Aβ deposits is not restricted to compounds that directly bind Aβ. The neuroprotective actions of KP, CRH, and catalase were confirmed in vitro, and fibrillar Aβ preparations were shown to stimulate the release of KP in vitro. In conclusion, neuroprotective KP, CRH, and catalase all colocalize with Aβ plaque-like deposits in the pons region from a male AD subject. </p>","PeriodicalId":16405,"journal":{"name":"Journal of Neurodegenerative Diseases","volume":"2013 ","pages":"879710"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/879710","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34129118","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":"P-Glycoprotein Altered Expression in Alzheimer's Disease: Regional Anatomic Variability.","authors":"Brian Jeynes, John Provias","doi":"10.1155/2013/257953","DOIUrl":"10.1155/2013/257953","url":null,"abstract":"<p><p>We investigated the expression of P-glycoprotein (P-gp) in brain samples of Alzheimer disease (AD) and normative brains (NM). Superior temporal cortex hippocampal and brainstem samples from 15 AD and NM brains were selected from comparable sites. P-gp positive capillaries and β-amyloid (Aβ) senile plaques (SP) were counted. Statistical analysis of the data was performed using nonparametric data analysis with Mann-Whitney, Kruskal-Wallis, and Spearman's tests. There were no significant differences in P-gp expression between superior temporal and hippocampus samples. However, there were significant differences in P-gp expression, when comparing brainstem with both hippocampal and superior temporal samples in both conditions (P < 0.012; P < 0.002 in NM cases and P < 0.001; <0.001 in AD cases); the brainstem has greater P-gp expression in each case and condition. In addition, there was a notable inverse negative correlation (P < 0.01) between P-gp expression and the presence of SPs in the AD condition superior temporal cortex. The results of this study suggest that there were significant site-dependent differences in the expression of P-gp. There may be an increased protective role for P-gp expression against amyloid deposition in the brainstem and in the superior temporal cortex of AD brains. </p>","PeriodicalId":16405,"journal":{"name":"Journal of Neurodegenerative Diseases","volume":"2013 ","pages":"257953"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4437351/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33957295","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":"Outcomes of a Peer Support Program in Multiple Sclerosis in an Australian Community Cohort: A Prospective Study.","authors":"Louisa Ng, Bhasker Amatya, Fary Khan","doi":"10.1155/2013/429171","DOIUrl":"https://doi.org/10.1155/2013/429171","url":null,"abstract":"<p><p>Background/Objectives. This pilot study evaluated the impact of a peer support program on improving multiple sclerosis (MS) related psychological functions (depression, anxiety, and stress) and enhancing quality of life. Methodology. Participants (n = 33) were recruited prospectively and received an 8-week group face-to-face peer support program. Assessments were at baseline (T1), 6 weeks after program (T2), and 12 months after program (T3), using validated questionnaires: Depression Anxiety Stress Scale (DASS), McGill Quality of Life (MQOL), and Brief COPE. Results. Participants' mean age was 52; the majority were female (64%) and married (64%). Median time since MS diagnosis was 16 years. At T2, participants reported improved psychological functioning (DASS \"depression,\" \"anxiety,\" and \"stress\" subscales, z values -2.36, -2.22, and -2.54, moderate effect sizes (r) 0.29, 0.28, and 0.32, resp.) and quality of life (MQOL SIS z score -2.07, r = 0.26) and were less likely to use \"self-blame\" as a coping mechanism (Brief COPE z score -2.37, r = 0.29). At T3, the positive improvements in stress (DASS stress subscale z score -2.41, r = 0.31) and quality of life were maintained (MQOL SIS, z score -2.30, r = 0.29). There were no adverse effects reported. </p>","PeriodicalId":16405,"journal":{"name":"Journal of Neurodegenerative Diseases","volume":"2013 ","pages":"429171"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/429171","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33957299","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}