| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Neurogenomics, Translational Genomics Research Institute, Phoenix, Arizona, United States
2 Sun Health Research Institute, Sun City, Arizona, United States; Psychology, Arizona State University, Tempe, Arizona, United States
3 Sun Health Research Institute, Sun City, Arizona, United States
4 Neurology, Mayo Clinic, Scottsdale, Arizona, United States
5 National Alzheimer's Coordinating Center, Seattle, Washington, United States
6 Washington University Alzheimer's Disease Research Center, St. Louis, Missouri, United States
7 Duke University Alzheimer's Disease Research Center, Durham, North Carolina, United States
8 Psychology, Arizona State University, Tempe, Arizona, United States
* To whom correspondence should be addressed. E-mail: dstephan{at}tgen.org.
In this article, we have characterized and compared gene expression profiles from laser capture microdissected neurons in six functionally and anatomically distinct regions from clinically and histopathologically normal aged human brains. These regions, which are also known to be differentially vulnerable to the histopathological and metabolic features of Alzheimer’s Disease (AD), include the entorhinal cortex and hippocampus (limbic and paralimbic areas vulnerable to early neurofibrillary tangle pathology in AD), posterior cingulate cortex (a paralimbic area vulnerable to early metabolic abnormalities in AD), temporal and prefrontal cortex (unimodal and heteromodal sensory association areas vulnerable to early neuritic plaque pathology in AD), and primary visual cortex (a primary sensory area relatively spared in early AD). These neuronal profiles will provide valuable reference information for future studies of the brain, in normal aging, AD and other neurological and psychiatric disorders.
This article has been cited by other articles:
|
|
 |
|
  F Skorpen, E. Laugsand, P Klepstad, and S Kaasa Variable response to opioid treatment: any genetic predictors within sight? Palliative Medicine, June 1, 2008; 22(4): 310 - 327. [Abstract] [PDF]
|
|
|
|
 |
|
 W. S. Liang, T. Dunckley, T. G. Beach, A. Grover, D. Mastroeni, K. Ramsey, R. J. Caselli, W. A. Kukull, D. McKeel, J. C. Morris, et al. Altered neuronal gene expression in brain regions differentially affected by Alzheimer's disease: a reference data set Physiol Genomics, April 1, 2008; 33(2): 240 - 256. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. S. Liang, E. M. Reiman, J. Valla, T. Dunckley, T. G. Beach, A. Grover, T. L. Niedzielko, L. E. Schneider, D. Mastroeni, R. Caselli, et al. Alzheimer's disease is associated with reduced expression of energy metabolism genes in posterior cingulate neurons PNAS, March 18, 2008; 105(11): 4441 - 4446. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
