Caitlin M Daimon, Patrick Chirdon, Stuart Maudsley, Bronwen Martin
{"title":"The role of Thyrotropin Releasing Hormone in aging and neurodegenerative diseases.","authors":"Caitlin M Daimon, Patrick Chirdon, Stuart Maudsley, Bronwen Martin","doi":"10.7726/ajad.2013.1003","DOIUrl":"10.7726/ajad.2013.1003","url":null,"abstract":"<p><p>Thyrotropin releasing hormone (TRH) is primarily known as the central regulator of the hypothalamic-pituitary-thyroid (HPT) axis. However, TRH also exerts a variety of central nervous system effects independent from its activity in the HPT axis. With advancing age, decreases in TRH synthesis, expression, and activity have been demonstrated. Associated with this emerging evidence suggests that TRH is implicated in neurodegenerative diseases of aging, including Alzheimer's disease and Parkinson's disease. TRH and its synthetic analogs have been recognized as trophic factors in neurons of the diencephalon and spinal cord, and as neuroprotectants against oxidative stress, glutamate toxicity, caspase-induced cell death, DNA fragmentation, and inflammation. In this review, we will provide an overview of some of the roles of TRH, outside of the HPT axis, associated with pathological aging and neurodegeneration and we shall discuss the potential of TRH and TRH analogs for the treatment of neurodegenerative diseases.</p>","PeriodicalId":89883,"journal":{"name":"American journal of Alzheimer's disease (Columbia, Mo.)","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3817016/pdf/nihms501267.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31839647","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}
Shanshan Li, Ozioma Okonkwo, Marilyn Albert, Mei-Cheng Wang
{"title":"Variation in Variables that Predict Progression from MCI to AD Dementia over Duration of Follow-up.","authors":"Shanshan Li, Ozioma Okonkwo, Marilyn Albert, Mei-Cheng Wang","doi":"10.7726/ajad.2013.1002","DOIUrl":"https://doi.org/10.7726/ajad.2013.1002","url":null,"abstract":"<p><p>The purpose of this paper is to investigate the relative utility of using neuroimaging, genetic, cerebrospinal fluid (CSF), and cognitive measures to predict progression from mild cognitive impairment (MCI) to Alzheimer's disease (AD) dementia over a follow-up period. The studied subjects were 139 persons with MCI enrolled in the Alzheimer's Disease Neuroimaging Initiative. Predictors of progression to AD included brain volume, ventricular volume, hippocampal volume, APOE ε4 two alleles, Aβ<sub>42</sub>, p-tau<sub>181</sub>, p-tau<sub>181</sub>/Aβ<sub>42</sub>, memory, language, and executive function. We employ a combination of Cox regression analyses and time-dependent receiver operating characteristic (ROC) methods to assess the prognostic utility and performance stability of candidate biomarkers. In a demographic-adjusted multivariable Cox model, seven measures- brain volume, hippocampal volume, ventricular volume, APOE ε4 two alleles, Aβ<sub>42</sub>, Memory composite, Executive function composite - predicted progression to AD. Time-dependent ROC revealed that this multivariable model had an area under the curve of 0.832, 0.788, 0.794, and 0.757 at 12, 18, 24, and 36 months respectively. Supplemental Cox models with time of origin set differentially at 12, 18, 24 and 36 months showed that six measures were significant predictors at 12 months whereas only memory and executive function predicted progression to AD at 18 and 24 months. The authors concluded that baseline volumetric MRI and cognitive measures selectively predict progression from MCI to AD, with cognitive measures remaining predictive even late in the follow-up period. These findings may inform case selection for AD clinical trials.</p>","PeriodicalId":89883,"journal":{"name":"American journal of Alzheimer's disease (Columbia, Mo.)","volume":"2 1","pages":"12-28"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.7726/ajad.2013.1002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32115582","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}
Jennifer A Eastman, Kristy S Hwang, Andreas Lazaris, Nicole Chow, Leslie Ramirez, Sona Babakchanian, Ellen Woo, Paul M Thompson, Liana G Apostolova
{"title":"Cortical thickness and semantic fluency in Alzheimer's disease and mild cognitive impairment.","authors":"Jennifer A Eastman, Kristy S Hwang, Andreas Lazaris, Nicole Chow, Leslie Ramirez, Sona Babakchanian, Ellen Woo, Paul M Thompson, Liana G Apostolova","doi":"10.7726/ajad.2013.1006","DOIUrl":"https://doi.org/10.7726/ajad.2013.1006","url":null,"abstract":"<p><p>The hallmark of Alzheimer's disease (AD) is declarative memory loss, but deficits in semantic fluency are also observed. We assessed how semantic fluency relates to cortical atrophy to identify specific regions that play a role in the loss of access to semantic information. Whole-brain structural magnetic resonance imaging (MRI) data were analyzed from 9 Normal Control (NC)(<i>M</i>=76.7, <i>SD</i>=5.6), 40 Mild Cognitive Impairment (MCI) (<i>M</i>=74.4, <i>SD</i>=8.6), and 10 probable AD (<i>M</i>=72.4, <i>SD</i>=8.0) subjects from the Alzheimer's Disease Neuroimaging Initiative (ADNI). They all were administered the Category Fluency (CF) animals and vegetables tests. Poorer semantic fluency was associated with bilateral cortical atrophy of the inferior parietal lobule (Brodman areas (BA) 39 and 40) and BA 6, 8, and 9 in the frontal lobe, as well as BA 22 in the temporal lobe. More diffuse frontal associations were seen in the left hemisphere involving BA 9, 10, 32, 44, 45, and 46. Additional cortical atrophy was seen in the temporoparietal (BA 37) and the right parastriate (BA 19, 18) cortices. Associations were more diffuse for performance on vegetable fluency than animal fluency. The permutation-corrected map-wise significance for CF animals was p<sub>corrected</sub>=0.01 for the left hemisphere, and p<sub>corrected</sub>=0.06 for the right hemisphere. The permutation-corrected map-wise significance for CF vegetables was p<sub>corrected</sub>=0.009 for the left hemisphere, and p<sub>corrected</sub>=0.03 for the right hemisphere. These results demonstrate the profound effect of cortical atrophy on semantic fluency. Specifically, tapping into semantic knowledge involves the frontal lobe in addition to the language cortices of the temporoparietal region.</p>","PeriodicalId":89883,"journal":{"name":"American journal of Alzheimer's disease (Columbia, Mo.)","volume":"1 2","pages":"81-92"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4207059/pdf/nihms594440.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32772529","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}