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Status |
Public on Feb 15, 2018 |
Title |
RNAseq of cortex of 6-month old APPPS1 and APPPS1;Apoe-/- mice |
Organism |
Mus musculus |
Experiment type |
Expression profiling by high throughput sequencing
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Summary |
One of the hallmarks of Alzheimer’s disease is the presence of extracellular diffuse and fibrillar plaques predominantly consisting of the amyloid-β (Aβ) peptide. ApoE influences the deposition of amyloid pathology through affecting the clearance and aggregation of monomeric Aβ in the brain. In addition to influencing Aβ metabolism, increasing evidence suggests that apoE influences microglial function in neurodegenerative diseases. Here, we characterize the impact that apoE has on amyloid pathology and the innate immune response in APPPS1∆E9 and APPPS1-21 transgenic mice. We report that Apoe deficiency reduced fibrillar plaque deposition consistent with previous studies. However, fibrillar plaques in Apoe-deficient mice exhibited a striking reduction in plaque compaction. Hyperspectral fluorescent imaging using luminescent conjugated oligothiophenes identified distinct Aβ morphotypes in Apoe-deficient mice. We also observed a significant reduction in fibrillar plaque-associated microgliosis and activated microglial gene expression in Apoe-deficient mice, along with significant increases in dystrophic neurites around fibrillar plaques. Our results suggest that apoE is critical in stimulating the innate immune response to amyloid pathology.
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Overall design |
Assessed the cortical gene expression of 6-month old APPPS1-21;ApoE-/- (n=7) and APPPS1-21 mice (n=6).
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Contributor(s) |
Jason U, David H |
Citation(s) |
29483128 |
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Submission date |
Jan 31, 2018 |
Last update date |
Mar 21, 2019 |
Contact name |
Jason Ulrich |
E-mail(s) |
ulrichjd@wustl.edu
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Phone |
3142731657
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Organization name |
Washington University
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Street address |
425 S. Euclid
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City |
St. Louis |
ZIP/Postal code |
63110 |
Country |
USA |
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Platforms (1) |
GPL17021 |
Illumina HiSeq 2500 (Mus musculus) |
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Samples (13)
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Relations |
BioProject |
PRJNA432321 |
SRA |
SRP131850 |