scholarly journals Author Correction: Disturbance of phylogenetic layer-specific adaptation of human brain gene expression in Alzheimer's disease

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Natasha Andressa Nogueira Jorge ◽  
Uwe Ueberham ◽  
Mara Knobloch ◽  
Peter F. Stadler ◽  
Jörg Fallmann ◽  
...  
2014 ◽  
Vol 35 (9) ◽  
pp. 1961-1972 ◽  
Author(s):  
Nicole C. Berchtold ◽  
Marwan N. Sabbagh ◽  
Thomas G. Beach ◽  
Ronald C. Kim ◽  
David H. Cribbs ◽  
...  

2014 ◽  
Vol 6 (4) ◽  
pp. 39 ◽  
Author(s):  
Mariet Allen ◽  
Michaela Kachadoorian ◽  
Zachary Quicksall ◽  
Fanggeng Zou ◽  
High Chai ◽  
...  

2019 ◽  
Author(s):  
Ying-Wooi Wan ◽  
Rami Al-Ouran ◽  
Carl Grant Mangleburg ◽  
Tom V. Lee ◽  
Katherine Allison ◽  
...  

SUMMARYHuman brain transcriptomes can highlight biological pathways associated with Alzheimer’s disease (AD); however, challenges remain to link expression changes with causal triggers. We have examined 30 AD-associated, gene coexpression modules from human brains for overlap with 251 differentially-expressed gene sets from mouse brain RNA-sequencing experiments, including from models of AD and other neurodegenerative disorders. Human-mouse overlaps highlight responses to amyloid versus neurofibrillary tangle pathology and further reveal age- and sex-dependent expression signatures for AD progression. Human coexpression modules enriched for neuronal and/or microglial genes overlap broadly with signatures from mouse models of AD, Huntington’s disease, Amyotrophic Lateral Sclerosis, and also aging. Several human AD coexpression modules, including those implicated in the unfolded protein response and oxidative phosphorylation, were not activated in AD models, but instead were detected following other, unexpected mouse genetic manipulations. Our results comprise a powerful, cross-species resource and pinpoint experimental models for diverse features of AD pathophysiology from human brain transcriptomes.


Neurology ◽  
2012 ◽  
Vol 78 (Meeting Abstracts 1) ◽  
pp. S54.001-S54.001
Author(s):  
M. Allen ◽  
F. Zou ◽  
H. S. Chai ◽  
C. Younkin ◽  
J. Crook ◽  
...  

1991 ◽  
Vol 21 (4) ◽  
pp. 855-866 ◽  
Author(s):  
Paul J. Harrison ◽  
Amanda J. L. Barton ◽  
Abdolrahman Najlerahim ◽  
Brendan McDonald ◽  
R. Carl A. Pearson

SYNOPSISMessenger RNA (mRNA) is the key intermediate in the gene expression pathway. The amount of mRNA in Alzheimer's disease (AD) brains has been determined using in situ hybridization histochemistry (ISHH) to detect the poly(A) tails of polyadenylated mRNA (poly(A) + mRNA). On a regional basis, AD cases had significantly less poly(A) + mRNA than controls in hippocampus (field CA3) and cerebellum (granule cell layer). Analysis of constituent pyramidal neurons showed mean reductions per cell within AD hippocampus (field CA3) and temporal cortex, but not in visual cortex. Similar changes were seen in a small group of non-AD dementias. The finding of reduced poly(A) + mRNA content is another indication of the altered brain gene expression occurring in AD. It is proposed that measurement of poly(A) + mRNA may be valuable in identifying functionally impaired neuronal populations. The methodology also provides a means by which changes in the quantitative distribution of individual mRNAs can be determined relative to that of poly(A) + mRNA as a whole.


2019 ◽  
Vol 15 ◽  
pp. P1260-P1260
Author(s):  
Carl Grant Mangleburg ◽  
Ying-Wooi Wan ◽  
Rami Al-Ouran ◽  
Tom V. Lee ◽  
Katherine S. Allison ◽  
...  

1993 ◽  
Vol 679 (1 Markers of Ne) ◽  
pp. 178-187 ◽  
Author(s):  
JOHN R. DUGUID ◽  
CHRISTOPHER TRZEPACZ ◽  
THOMAS KEMPER ◽  
WALLACE W. TOURTELLOTE ◽  
LADISLAV VOLICER

2020 ◽  
Vol 11 (2) ◽  
pp. 8686-8701

The currently utilized neuroimaging and cerebrospinal fluid-based detection of Alzheimer’s disease (AD) suffer several limitations, including sensitivity, specificity, and cost. Therefore, the identification of AD by analyzing blood gene expression may ameliorate the early diagnosis of the AD. We aimed to identify common genes commonly deregulated in blood and brain in AD. Comprehensive analysis of blood and brain gene expression datasets of AD, eQTL, and epigenetics data was analyzed by the integrative bioinformatics approach. The integrative analysis showed nine differentially expressed genes common to blood cells and brain (CNBD1, SUCLG2-AS1, CCDC65, PDE4D, MTMR1, C3, SLC6A15, LINC01806, and FRG1JP). Analysis of SNP and cis-eQTL data showed 18 genes; namely, HSD17B1, GAS5, RPS5, VKORC1, GLE1, WDR1, RPL12, MORN1, RAD52, SDR39U1, NPHP4, MT1E, SORD, LINC00638, MCM3AP-AS1, GSDMD, RPS9, and GNL2 were observed deregulated AD blood and brain tissues. Functional gene set enrichment analysis demonstrated a significant association of these genes in neurodegeneration-associated molecular pathways. Integrative biomolecular networks revealed dysregulation of several hub transcription factors and microRNAs in AD. Moreover, hub genes were observed associated with significant histone modification. This study detected common molecular biomarkers and pathways in blood and brain tissues in AD that may be potential biomarkers and therapeutic targets in AD.


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