Incipient Alzheimer's disease: Microarray correlation analyses reveal major transcriptional and tumor suppressor responses

By E. Blalock, J. Geddes, K. Chen, N. Porter, W. Markesbery, P. Landfield. Proceedings of the National Academy of Sciences of the United States of America, 2004

1,072 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/68f6c4abeb600d0259b7b96cda72698505ed8232

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Citations in the corpus

Using control genes to correct for unwanted variation in microarray data. (2012, background): “2 Alzheimer’s Study Blalock et al. (2004) conducted a microarray study to investigate patterns of gene expression in Alzheimer’s patients.”
NOA: a novel Network Ontology Analysis method (2011, background): “This provides evidence for neuron cell death and protein degradation in the serious disease stage of AD (30).”
Mitochondrial bioenergetic deficit precedes Alzheimer's pathology in female mouse model of Alzheimer's disease (2009, background): “Increasing evidence implicates mitochondrial dysfunction in multiple neurodegenerative disorders (22).”
Decoding Alzheimer's disease from perturbed cerebral glucose metabolism: implications for diagnostic and therapeutic strategies. (2013, background): “AD brain tissues have been found to exhibit increase of expression or activity of GSK-3 (Blalock et al., 2004), and hence hyper-activation of GSK-3 could induce the apoptosis of cholinergic neurons (Hoshi et al.”
Systems biology and gene networks in neurodevelopmental and neurodegenerative disorders (2015, background): “…138,139 ; preclinical changes in at-risk individuals with a milder disease presentation can identify genes and pathways that might lead to disease 140 ; and cell type-specific markers can be used in combination with bioin-formatic analyses to account for the effect of changes in cell proportion…”
Progesterone receptors: form and function in brain. (2008, neutral): “In Alzheimer’s disease (AD), cell cycle-specific gene expression is upregulated [32] and, evidence indicates that mitotic signaling is dysregulated [305].”
Early remodeling of the neocortex upon episodic memory encoding (2014, background): “, upregulation of synaptic plasticity-related genes, down-regulation of immune-related genes) is the inverse of the gene expression profile characteristic of AD (52) (i.”
PathNet: a tool for pathway analysis using topological information (2012, neutral): “The first dataset (GEO ID: GDS810) [20], which we refer to as the disease progression dataset, investigated the expression profile of genes from the hippocampal region of the brain as a function of the progression of the disease (incipient, moderate, and severe).”
Inflammation in Alzheimer disease-a brief review of the basic science and clinical literature. (2012, background): “More recent support for activation of complement in AD comes from a number of transcriptome studies showing that complement gene expression is increased in the disease (Blalock et al. 2004; Katsel et al. 2009).”
The GSK3 hypothesis of Alzheimer's disease (2008, background): “Furthermore, GSK3 expression is up-regulated in the hippocampus of AD patients (Blalock et al. 2004) and in post-synaptosomal supernatants derived from AD brain (Pei et al. 1997), although the latter study reports that there is not an increase in GSK3 enzymatic activity.”