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Physiol. Genomics (February 12, 2008). doi:10.1152/physiolgenomics.00242.2007
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Submitted on October 12, 2007
Accepted on February 8, 2008

Altered neuronal gene expression in brain regions differentially affected by Alzheimer’s Disease: A reference data set

Winnie S Liang1, Travis Dunckley2, Thomas G Beach3, Andrew Grover4, Diego Mastroeni5, Keri Ramsey6, Richard J Caselli7, Walter A Kukull8, Daniel McKeel9, John C Morris9, Christine M. Hulette10, Donald Schmechel10, Eric M Reiman11, Joseph Rogers3, and Dietrich A. Stephan12*

1 Neurogenomics, Translational Genomics Research Institute, Phoenix, Arizona, United States; Arizona Alzheimer's Disease Consortium, Phoenix, Arizona, United States
2 Neurogenomics, Translational Genomics Research Institute, 85004, Arizona, United States; Arizona Alzheimer's Disease Consortium, 85006, Arizona, United States
3 Sun Health Research Institute, Sun City, Arizona, United States; Arizona Alzheimer's Disease Consortium, 85006, Arizona, United States
4 Sun Health Research Institute, 85006, Arizona, United States; Arizona Alzheimer's Disease Consortium, 85006, Arizona, United States
5 Sun Health Research Institute, Sun City, Arizona, United States
6 Neurogenomics, Translational Genomics Research Institute, Phoenix, Arizona, United States
7 Arizona Alzheimer's Disease Consortium, Phoenix, Arizona, United States
8 National Alzheimer's Coordinating Center, Seattle, Washington, United States
9 Washington University Alzheimer's Disease Research Center, 63108, Missouri, United States
10 Duke University Alzheimer's Disease Research Center, 27705, North Carolina, United States
11 Neurogenomics, Translational Genomics Research Institute, 85004, Arizona, United States
12 Neurogenomics, Translational Genomics Research Institute, Phoenix, Arizona, United States; Arizona Alzheimer's Disease Consortium, 85006, Arizona, United States

* To whom correspondence should be addressed. E-mail: dstephan{at}tgen.org.

Alzheimer’s Disease (AD) is the most widespread form of dementia during the later stages of life. If improved therapeutics are not developed, the prevalence of AD will drastically increase in the coming years as the world’s population ages. By identifying differences in neuronal gene expression profiles between healthy elderly persons and individuals diagnosed with AD, we may be able to better understand the molecular mechanisms that drive AD pathogenesis, including the formation of amyloid plaques and neurofibrillary tangles. In this study, we expression profiled histopathologically normal cortical neurons collected using laser capture microdissection (LCM) from 6 anatomically and functionally discrete post-mortem brain regions in 34 AD-afflicted individuals using Affymetrix Human Genome U133 Plus 2.0 microarrays. These regions include the entorhinal cortex, hippocampus, middle temporal gyrus, posterior cingulate cortex, superior frontal gyrus, and primary visual cortex. This study is predicated on previous parallel research on the post-mortem brains of the same 6 regions in 14 healthy elderly individuals, for which LCMed neurons were similarly processed for expression analysis. We identified significant regional differential expression in AD brains compared to controls including expression changes of genes previously implicated in AD pathogenesis particularly with regards to tangle and plaque formation. Pinpointing the expression of factors that may play a role in AD pathogenesis provides a foundation for future identification of new targets for improved AD therapeutics. We provide this carefully phenotyped, laser capture microdissected intra-individual brain region expression data set to the community as a public resource.




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