Genome wide profiling of altered gene expression in the neocortex of Alzheimer's disease
@article{Tan2010GenomeWP,
title={Genome wide profiling of altered gene expression in the neocortex of Alzheimer's disease},
author={Michelle Guet Khim Tan and Wei T Chua and Margaret M. Esiri and A David Smith and Harry V. Vinters and Mitchell Kim Peng Lai},
journal={Journal of Neuroscience Research},
year={2010},
volume={88}
}Alzheimer's disease (AD) is characterized by a complex neurodegenerative process affecting multiple genes and proteins in the neocortex, many of which have not been well‐studied. In this study, we investigated genome‐wide gene alterations in the temporal cortex of a well‐characterized cohort of AD patients using a recently developed microarray platform, and compared some of the transcript changes with immunoblotting. Of the 5485 genes found to be significantly altered in AD, there were…
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References
SHOWING 1-10 OF 73 REFERENCES
A gene expression profile of Alzheimer's disease.
- BiologyDNA and cell biology
- 2001
A gene expression profile for AD brain showed that 118 of the 7050 sequences on a broadly representative cDNA microarray were differentially expressed in the amygdala and cingulate cortex, two regions affected early in the disease.
A Systems Level Analysis of Transcriptional Changes in Alzheimer's Disease and Normal Aging
- BiologyThe Journal of Neuroscience
- 2008
The transcriptional network in AD was characterized, identifying 12 distinct modules related to synaptic and metabolic processes, immune response, and white matter, nine of which were related to disease progression, and presenilin 1 (PSEN1) is highly coexpressed with canonical myelin proteins, suggesting a role for PSEN1 in aspects of glial-neuronal interactions related to neurodegenerative processes.
Defects in expression of genes related to synaptic vesicle traffickingin frontal cortex of Alzheimer’s disease
- BiologyNeurobiology of Disease
- 2003
Expression profile of transcripts in Alzheimer's disease tangle‐bearing CA1 neurons
- BiologyAnnals of neurology
- 2000
The profile of mRNAs differentially expressed by tangle‐bearing CA1 neurons may represent a “molecular fingerprint” of these neurons, and it is speculated that mRNA expression profiles of diseased neurons in AD may suggest new directions for AD research or identify novel targets for developing more effective AD therapies.
Alzheimer's disease: mRNA expression profiles of multiple patients show alterations of genes involved with calcium signaling
- BiologyNeurobiology of Disease
- 2006
Incipient Alzheimer's disease: Microarray correlation analyses reveal major transcriptional and tumor suppressor responses
- BiologyProceedings of the National Academy of Sciences of the United States of America
- 2004
A new model of AD pathogenesis is suggested in which a genomically orchestrated up-regulation of tumor suppressor-mediated differentiation and involution processes induces the spread of pathology along myelinated axons.
Use of cDNA microarray in the search for molecular markers involved in the onset of Alzheimer's disease dementia
- BiologyJournal of neuroscience research
- 2001
Evidence supports the feasibility and usefulness of cDNA microarray techniques to study sequential changes of distinctive gene‐expression patterns in the brain as a function of the progression of AD dementia and suggests new means to dissect and classify stages ofAD dementia, or neuropathology, at the molecular level.
Transcriptome Analysis of Synaptoneurosomes Identifies Neuroplasticity Genes Overexpressed in Incipient Alzheimer's Disease
- BiologyPloS one
- 2009
A novel approach concentrates synaptic mRNA, thereby increasing the ratio of synaptic to somal mRNA and allowing discrimination of expression changes in synaptically localized genes, and implies a functional impact on synaptic transmission as GluR2, if inserted, maintains the receptors in a low conductance state.
Up-regulation of calcineurin Abeta mRNA in the Alzheimer's disease brain: assessment by cDNA microarray.
- BiologyBiochemical and biophysical research communications
- 2001
This study suggests that CAbeta may play a crucial role in the pathophysiological mechanisms in AD.