1,133 research outputs found
George Albert Goates, Wallace Albert Goates, Elizabeth Collis Munns, Louisa Munns Goates
Black and white photograph George Albert Goates, Wallace Albert Goates, Elizabeth Collis Munns, Louisa Munns Goate
Deseret News Obituary for Judge George Albert Goates
Text document, Obituary for Judge George Albert Goate
The Wallace Goates Family
Color photograph, Colorized- Left to right Top: Roma Louise Tolton Goates, Julie Maud May Goates, Bottom: Wallace Albert Goates, Romoa Tolton Goates, Delbert Tolton Goate
Marioni_et_al_AD_GWAS_Sumstats_June2019_Correction - Data supporting Marioni et al. "GWAS on family history of Alzheimer's disease"
Data supporting the paper: Marioni, RE, Harris, SE, Zhang, Q, Mcrae, AF, Hagenaars, SP, Hill, WD, Davies, G, Ritchie, CW, Gale, CR, Starr, JM, Goate, AM, Porteous, DJ, Yang, J, Evans, KL, Deary, IJ, Wray, NR & Visscher, PM 2018, 'GWAS on family history of Alzheimer’s disease' Translational Psychiatry, vol. 8, no. 1. DOI: 10.1038/s41398-018-0150-6.
## Note about using the files ##
Each of the .txt files contains over seven million rows. Users will encounter difficulties if they attempt to view the content using Notepad++ or Microsoft Notepad. Microsoft Excel 2016 will not display all rows. These space-delimited text files contains several columns, with a header row, which are listed in the readme file
Doktór Janusz Korczak
This historical poster is a portrait of Doktór Janusz Korczak (1878-1942).portrait of bald man with goate
Ubiquilin 1 polymorphisms are not associated with late-onset Alzheimer's disease
Several studies have reported evidence for linkage of late-onset Alzheimer's disease (LOAD) to chromosome 9. Recently, an intronic polymorphism affecting alternative splicing of exon 8 of ubiquilin 1 (UBQLN1) was reported to be associated with LOAD. We attempted to replicate this observation by genotyping this polymorphism, rs12344615 (also known as UBQ-8i), in a large sample of 1,544 LOAD cases and 1,642 nondemented controls. We did not find any evidence that this single nucleotide polymorphism, or any of six others tested in UBQLN1, increases risk for LOAD.
Williams J, Goate A
Marioni_et_al_AD_GWAS_Sumstats_June2019_Correction - Data supporting Marioni et al. "GWAS on family history of Alzheimer's disease"
Data supporting the paper: Marioni, RE, Harris, SE, Zhang, Q, Mcrae, AF, Hagenaars, SP, Hill, WD, Davies, G, Ritchie, CW, Gale, CR, Starr, JM, Goate, AM, Porteous, DJ, Yang, J, Evans, KL, Deary, IJ, Wray, NR & Visscher, PM 2018, 'GWAS on family history of Alzheimer’s disease' Translational Psychiatry, vol. 8, no. 1. DOI: 10.1038/s41398-018-0150-6. ## Note about using the files ## Each of the .txt files contains over seven million rows. Users will encounter difficulties if they attempt to view the content using Notepad++ or Microsoft Notepad. Microsoft Excel 2016 will not display all rows. These space-delimited text files contains several columns, with a header row, which are listed in the readme file.Marioni, Riccardo; Harris, Sarah; Zhang, Qian; McRae, Allan; Hagenaars, Saskia; Hill, David; Davies, Gail; Ritchie, Craig; Gale, Catharine; Starr, John; Goate, Alison; Porteous, David; Yang, Jian; Evans, Kathy; Deary, Ian; Wray, Naomi; Visscher, Peter. (2019). Marioni_et_al_AD_GWAS_Sumstats_June2019_Correction - Data supporting Marioni et al. "GWAS on family history of Alzheimer's disease", [dataset]. University of Edinburgh. Centre for Cognitive Ageing and Cognitive Epidemiology. https://doi.org/10.7488/ds/2578
rs5848 variant influences GRN mRNA levels in brain and peripheral mononuclear cells from patients with Alzheimer's disease
Mutations in the progranulin gene (GRN), causative for Frontotemporal Lobar Degeneration with ubiquitin-immunoreactive neuronal inclusions (FTLD-U), could also be associated with Alzheimer's disease (AD). The influence of GRN genetic variability on susceptibility to AD and on expression levels in a series of neuropathologically-confirmed AD patients as well as in peripheral mononuclear cells (PBMC) and in cells isolated from cerebrospinal fluid (CSF) was investigated. An association study of rs9897526 and rs5848 was carried out in an Italian population and in a replication population of European American patients and controls. None of the variants tested act as unequivocal susceptibility factor in both populations although rs9897526 anticipated the onset of the disease in the Italian population. GRN expression in the parietal lobe of AD cases showed a 0.76-fold decrease compared with controls (1.31 +/- 0.07 versus 1.73 +/- 0.12, P = 0.0025). Patients carrying the rs5848 TT genotype had the lowest GRN expression levels (0.96 +/- 0.12, P = 0.014). Despite no significant differences were found in the relative PBMC and CSF GRN expression in patients compared to controls, stratifying patients according to the presence of rs5848 T allele, a 0.57-fold decrease in GRN mRNA levels over C carriers was found in PBMC (1.22 +/- 0.23 versus 0.70 +/- 0.12, P = 0.04). Similarly to data obtained in brain samples, patients carrying the TT genotype showed the lowest GRN mRNA levels (TT = 0.46 +/- 0.14, CC = 1.22 +/- 0.23; P = 0.013). These data argue against a direct role of GRN as a susceptibility factor for sporadic AD but support a role of GRN as a disease-modifying gene, possibly contributing to the failure of neuronal survival
An Efficient Platform for Astrocyte Differentiation from Human Induced Pluripotent Stem Cells
Summary: Growing evidence implicates the importance of glia, particularly astrocytes, in neurological and psychiatric diseases. Here, we describe a rapid and robust method for the differentiation of highly pure populations of replicative astrocytes from human induced pluripotent stem cells (hiPSCs), via a neural progenitor cell (NPC) intermediate. We evaluated this protocol across 42 NPC lines (derived from 30 individuals). Transcriptomic analysis demonstrated that hiPSC-astrocytes from four individuals are highly similar to primary human fetal astrocytes and characteristic of a non-reactive state. hiPSC-astrocytes respond to inflammatory stimulants, display phagocytic capacity, and enhance microglial phagocytosis. hiPSC-astrocytes also possess spontaneous calcium transient activity. Our protocol is a reproducible, straightforward (single medium), and rapid (<30 days) method to generate populations of hiPSC-astrocytes that can be used for neuron-astrocyte and microglia-astrocyte co-cultures for the study of neuropsychiatric disorders. : Brennand, Goate, and colleagues report a rapid and robust method for the differentiation of highly pure populations of replicative astrocytes from human induced pluripotent stem cells (hiPSCs) via a neural progenitor cell (NPC) intermediate. hiPSC-astrocytes resemble primary human fetal astrocytes, have a transcriptional signature consistent with a non-reactive state, respond to inflammatory stimulants, and enhance microglial phagocytosis. Keywords: human induced pluripotent stem cell, iPSC, astrocyt
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