Gene expression profiling of 12633 genes in Alzheimer hippocampal CA1: transcription and neurotrophic factor down-regulation and up-regulation of apoptotic and pro-inflammatory signaling
Open accessAbstract
Alterations in transcription, RNA editing, translation, protein processing, and clearance are a consistent feature of Alzheimer's disease (AD) brain. To extend our initial study (Alzheimer Reports [2000] 3:161-167), RNA samples isolated from control and AD hippocampal cornu ammonis 1 (CA1) were analyzed for 12633 gene and expressed sequence tag (EST) expression levels using DNA microarrays (HG-U95Av2 Genechips; Affymetrix, Santa Clara, CA). Hippocampal CA1 tissues were carefully selected from several hundred potential specimens obtained from domestic and international brain banks. To minimize the effects of individual differences in gene expression, RNA of high spectral quality (A(260/280) > or= 1.9) was pooled from CA1 of six control or six AD subjects. Results were compared as a group; individual gene expression patterns for the most-changed RNA message levels were also profiled. There were no significant differences in age, postmortem interval (mean < or = 2.1 hr) nor tissue pH (range 6.6-6.9) between the two brain groups. AD tissues were derived from subjects clinically classified as CDR 2-3 (CERAD/NIA). Expression data were analyzed using GeneSpring (Silicon Genetics, Redwood City, CA) and Microarray Data Mining Tool (Affymetrix) software. Compared to controls and 354 background/alignment markers, AD brain showed a generalized depression in brain gene transcription, including decreases in RNA encoding transcription factors (TFs), neurotrophic factors, signaling elements involved in synaptic plasticity such as synaptophysin, metallothionein III, and metal regulatory factor-1. Three- or morefold increases in RNAs encoding DAXX, cPLA(2), CDP5, NF-kappaBp52/p100, FAS, betaAPP, DPP1, NFIL6, IL precursor, B94, HB15, COX-2, and CEX-1 signals were strikingly apparent. These data support the hypothesis of widespread transcriptional alterations, misregulation of RNAs involved in metal ion homeostasis, TF signaling deficits, decreases in neurotrophic support and activated apoptotic and neuroinflammatory signaling in moderately affected AD hippocampal CA1.
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B94 is a TNF-α-inducible proinflammatory element.
“B94 (GenBank M92357) is a TNF-α-inducible proinflammatory element (Colangelo et al., 2002; Liao et al., 2004).”
From Docosanoids and elovanoids from omega-3 fatty acids are pro-homeostatic modulators of inflammatory responses, cell damage and neuroprotection (2018) · cites this paper as Colangelo et al., 2002
CEX-1 is a marker for inflammatory and oxidative stress responses.
“CEX-1 (GenBank U64197) is a marker for inflammatory and oxidative stress responses (Colangelo et al., 2002; McGeer and McGeer, 2003),”
From Docosanoids and elovanoids from omega-3 fatty acids are pro-homeostatic modulators of inflammatory responses, cell damage and neuroprotection (2018) · cites this paper as Colangelo et al., 2002
Intersection of the microglia signature gene list with 46 publicly available data sets for differentially regulated genes in neurodegenerative and behavioral disorders revealed significant enrichment or depletion of microglia signature genes in 28 of the 46 data sets.
“We then intersected this gene list with 46 publicly available data sets for differentially regulated genes in neurodegenerative and behavioral disorders derived from microarray or RNA-seq analysis of intact tissue (39–53). Two-sided Fisher’s exact tests revealed significant enrichment or depletion of microglia signature genes in 28 of the 46 data sets (Table S3).”
From An environment-dependent transcriptional network specifies human microglia identity (2017) · cites this paper as [42]
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“[27]; (4) Liang, signature detected in multiple cortex areas from Liang et al.”
Background
- Authors
- Colangelo, V., Schurr, J., Ball, M. J., Pelaez, R. P., Bazan, N. G., & Lukiw, W. J.
- Affiliations
- Louisiana State University Health Sciences Center New Orleans (US)
- Oregon Health & Science University (US)
- Corresponding author
- Lukiw, Walter J.
- Venue
- Journal of Neuroscience Research
- Publisher
- Wiley
- Published
- 2002-10-18
- Volume
- 70
- Issue
- 3
- Pages
- 462-473
- ISSN
- 0360-4012 (ISSN-L)
- 1097-4547
- OpenAlex
- W1977813572
- Cited by
- 517
- References
- 75
- Citations by year
- 2026: 6 · 2025: 3 · 2024: 4 · 2023: 15 · 2022: 22 · 2021: 16 · 2020: 14 · 2019: 13 · 2018: 15 · 2017: 15 · 2016: 29 · 2015: 25 · 2014: 28 · 2013: 23 · 2012: 19
- FWCI
- 19.18
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neuroscience Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- U.S. Public Health Service
- National Institute on Aging (AG 08017, P30AG008017, AG18031, R01AG018031)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, hippocampal CA1, gene expression profiling, transcriptional downregulation, neurotrophic factors, apoptosis, neuroinflammation, NF-κB signaling, metal homeostasis, metallothionein, synaptophysin, cyclooxygenase-2, Fas, amyloid precursor protein, DAXX
- MeSH terms
- Aged, Alzheimer Disease, Encephalitis, Female, Gene Expression Regulation, Hippocampus, Homeostasis, Humans, Male, Nerve Growth Factors, Transcription Factors, Signal Transduction, Down-Regulation, Up-Regulation, Apoptosis, DNA, Complementary, Oligonucleotide Array Sequence Analysis
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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