Transcriptomics,Genomics

Dataset Information

33

Expression data from C57/6J mice (Normal), APP/PS1 mice and APP/PS1 mice treatment with HPYD


ABSTRACT: Aβ is a peptide of 39-42 amino acid residues that derived from putative intramembranous processing of amyloid precursor protein (APP) at the proposed active site of the γ-secretase/PS1 aspartyl. Aβ has been shown to aggregate and accumulate abnormally in the brain of AD (Alzheimer's disease), and extracellular amyloid plaques of Aβ peptides aggregation can trigger a cascade of pathologic events leading to nerve fiber entanglement and neuronal apoptosis protease. We used microarrays to investigate the effects of HPYD on the gene expression of APP/PS1 transgenic mice, the brain tissues of control group, model group and HPYD group mice. Overall design: The brain tissues of control group (Normal mice), model group (APP/PS1 mice) and HPYD group mice were obtained from the mice at the end of the Morris water maze experiment. The total RNAs from these brain tissues were isolated for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain the expression profiles of control group , model group and HPYD group mice, and found the dysregulated expression of many genes in model mice that could be restored to normal level after treatment with HPYD according to three groups:control group, model group and HPYD group.

INSTRUMENT(S): [MoGene-1_0-st] Affymetrix Mouse Gene 1.0 ST Array [transcript (gene) version]

SUBMITTER: Weiying Liu  

PROVIDER: GSE104249 | GEO | 2018-02-23

REPOSITORIES: GEO

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Publications

β-Sheet Breaker Peptide-HPYD for the Treatment of Alzheimer's Disease: Primary Studies on Behavioral Test and Transcriptional Profiling.

Liu Weiying W   Sun Fengxian F   Wan Moxin M   Jiang Fang F   Bo Xiangyu X   Lin Laixiang L   Tang Hua H   Xu Shumei S  

Frontiers in pharmacology 20170101


Background: Alzheimer's disease (AD), is a progressive neurodegenerative disease that is characterized by cognitive loss. Most researchers believe that aggregation and accumulation of β-amyloid peptides (Aβ) in brain cells are the central pathological hallmark of this disease. Methods: Based on the amyloid hypothesis, a 10 amino acids β-sheet breaker peptide HPYD (His-Lys-Gln-Leu-Pro-Phe-Tyr-Glu-Glu-Asp) was designed according to the structure and sequence of the previous designed peptide H102.  ...[more]

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