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Status |
Public on Feb 08, 2018 |
Title |
Comparative Transcriptomics of Choroid Plexus in Alzheimer's Disease, Huntington's Disease and Frontotemporal Dementia: Implications for CSF Homeostasis and Dynamics |
Organism |
Homo sapiens |
Experiment type |
Expression profiling by array
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Summary |
Background: In aging and Alzheimer’s disease there are striking changes in CSF composition that may relate to altered choroid plexus function. Studying CP tissue gene expression at the BCSFB provides further insight into epithelial and stromal responses to aging and diseased states. Results: Highly significant differences in gene expression occurred in CP of advanced AD patients vs. normal controls. Immune-related pathways including acute phase response, cytokine/JAK/STAT signaling and cell adhesion were the most significantly enriched among the genes upregulated in AD patients, while methionine degradation, and protein translation genes were most notably downregulated. While the majority of gene expression changes in AD patients was also observed in FTD and HuD, there were significant differences among the disease groups. AD had the most unique expression findings, these genes being enriched in upregulated VEGF signaling and immune response proteins, e.g., interleukins. HuD/FTD patients uniquely displayed upregulated cadherin-mediated adhesion. Conclusions: This unique database of changes in CP tissue gene expression provides mechanistic insight into the effects of neurodegenerative diseases on CSF dynamics and hydrocephalus, particularly in regards to choroidal immune activation, metabolic homeostasis and resiliency of the CP.
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Overall design |
Methods: Transcriptome-wide Affymetrix microarrays were used to determine disease-related changes in gene expression within human choroid plexus. Post-mortem tissue samples of the entire lateral ventricular choroid plexus were from 6 healthy controls and 7 patients with advanced (Braak & Braak stage III-VI) Alzheimer’s disease (AD), 4 with Frontotemporal dementia (FTD) and 3 with Huntington’s disease (HuD).
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Contributor(s) |
Stopa EG, Tanis KQ, Miller MC, Nikonova EV, Podtelezhnikov AA, Finney EM, Stone DJ, Camargo LM, Parker L, Verma A, Baird A, Donahue JE, Torabi T, Eliceiri B, Silverberg GD, Klinge PM, Johanson CE |
Citation(s) |
29848382, 30541599 |
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Submission date |
Feb 06, 2018 |
Last update date |
Dec 26, 2018 |
Contact name |
Edward G Stopa |
E-mail(s) |
estopa@lifespan.org
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Organization name |
Brown University
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Department |
Pathology & Laboratory Medicine
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Lab |
Division of Neuropathology
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Street address |
593 Eddy Street
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City |
Providence |
State/province |
RI |
ZIP/Postal code |
02903 |
Country |
USA |
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Platforms (1) |
GPL10379 |
Rosetta/Merck Human RSTA Custom Affymetrix 2.0 microarray [HuRSTA-2a520709] |
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Samples (20)
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Relations |
BioProject |
PRJNA433420 |
Supplementary file |
Size |
Download |
File type/resource |
GSE110226_RAW.tar |
123.8 Mb |
(http)(custom) |
TAR (of CEL) |
Processed data included within Sample table |
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