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Series GSE13214 Query DataSets for GSE13214
Status Public on Jan 11, 2013
Title Evaluation of gene expression profile in postmortem brain with Alzheimer´s disease-type neuropathological changes
Organism Homo sapiens
Experiment type Expression profiling by array
Summary Unravel the mechanisms underlying brain aging and Alzheimer´s disease (AD) has been difficult because of complexity of the networks that drive these aging-related changes. Analysis of the gene expression in the brain is a valuable tool to study the function of the brain under normal and pathological conditions. Gene microarray technology allows massively parallel analysis of most genes expressed in a tissue, and therefore is an important research tool that potentially can provide the investigative power needed to address the complexity of brain aging and neurodegenerative processes. One of the reasons that account for the resistance of AD pathogenesis to analysis is that clinically normal subjects may exhibit considerable AD pathology, blurring criteria for distinguishing subjects with normal aging or AD. Here, we analyzed hippocampal and cortex frontal gene expression from 32 subjects separated in individuals presenting, 1) both pathologic and clinical AD (definitive AD); 2) AD pathology and normal clinic (pathologic AD); 3) cognitive impairment, without AD pathology (others dementias); and 4) no cognitive impairment, without AD pathology (normal individuals). Our results show that based on gene expression profile these individuals we could verify similarity between the definitive AD group and the group that only had AD-type pathology (pathologic AD).
 
Overall design Specimens of hippocampus and cortex frontal used in this study were obtained at autopsy from 32 subjects. Neuropathology, specifically NFT and NP, was assessed in accordance to the Braak staging and CERAD scores, respectively. Based on pathologic and clinic criteria, subjects were categorized into four groups: 1) nine subjects with AD neuropathologic (Braak = IV / V / VI and CERAD ≠ 0) presenting cognitive impairment (CDR ≥ 1), termed “definitive AD” (dAD); 2) five subjects with AD neuropathologic (Braak = IV / V / VI and CERAD ≠ 0) and without cognitive impairment (CDR = 0), termed “pathologic AD” (pAD); 3) nine subjects without AD neuropathologic (Braak = 0 / I / II and CERAD ≠ C) presenting cognitive impairment (CDR ≥ 1), termed “other dementias” (OD); 4) - nine subjects without AD neuropathologic (Braak = 0 / I / II and CERAD ≠ C) and without cognitive impairment (CDR = 0), termed “normal” (N). RNA isolation and Amplification. From total RNA, a two-round linear amplification procedure (T7-based protocol) was carried out for all samples and for a pool of RNAs
obtained from 15 distinct human cell lines used as reference. Labeled cDNA was generated in a reverse transcriptase reaction using amplified RNA (aRNA). Equal amounts of test and reference cDNA reverse color Cy-labeled aRNA targets were competitively hybridized against the cDNA probes in a customized cDNA platform with 4,608 ORESTES representing human genes. Dye-swap was performed for each sample as control for dye bias and used as replicate.
 
Contributor(s) Silva AR, Brentani H
Citation(s) 23144955, 27213057
Submission date Oct 15, 2008
Last update date Oct 04, 2019
Contact name Renato David Puga
Organization name Universidade de São Paulo
Department Instituto de Psiquiatria
Lab Laboratório de Genética
Street address Dr Ovidio Pires de Campos,785
City São Paulo
State/province São Paulo
ZIP/Postal code 05403-010
Country Brazil
 
Platforms (1)
GPL1930 Homo sapiens 4.8K 02-01 amplified cDNA
Samples (128)
GSM333463 definitive_Alzheimer_8_frontal_cortex_rep1
GSM333464 definitive_Alzheimer_8_frontal_cortex_rep2
GSM333465 definitive_Alzheimer_8_hippocampus_rep1
Relations
BioProject PRJNA109447

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Supplementary data files not provided
Processed data included within Sample table
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