Altered neuronal gene expression in brain regions differentially affected by Alzheimer's disease: a reference data set
Open accessAbstract
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 with laser capture microdissection (LCM) from six anatomically and functionally discrete postmortem 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 postmortem brains of the same six regions in 14 healthy elderly individuals, for which LCM neurons were similarly processed for expression analysis. We identified significant regional differential expression in AD brains compared with control brains including expression changes of genes previously implicated in AD pathogenesis, particularly with regard 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 intraindividual brain region expression data set to the community as a public resource.
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The first large transcriptomic study (188 controls and 176 Alzheimer disease cases) connected genetic variation to expression changes using eQTL analysis and supported pathway-level findings related to transcriptional regulation and energy metabolism.
“The first large transcriptomic study (involving 188 controls and 176 individuals with Alzheimer disease)147 connected genetic variation to expression changes by using expression quantitative trait locus analysis (eQTL analysis) in controls and Alzheimer disease, and further supported the pathway-level findings related to transcriptional regulation and energy metabolism in Alzheimer disease140,148.”
From Systems biology and gene networks in neurodevelopmental and neurodegenerative disorders (2015) · cites this paper as [148]
Adult PTB expression was found in human laser capture microdissected ECII neurons and in diverse brain regions in GTEx.
“Furthermore, we analyzed transcriptomic data from laser capture microdissected ECII neurons in humans (Liang et al., 2008) and from diverse brain regions in GTEx (GTEx consortium) and found adult PTB expression in both (Figure S3B).”
From Selective Neuronal Vulnerability in Alzheimer’s Disease: A Network-Based Analysis (2020) · cites this paper as Liang et al., 2008
NetWAS 2.0 predictions were very significantly enriched in genes differentially downregulated in ECII neurons of sporadic Alzheimer's disease patients (one-sided Wilcoxon rank-sum test, p-value < 2.2×10−16).
“Furthermore, our predictions were very significantly enriched in genes differentially downregulated in ECII neurons of sporadic AD patients measured in a different study (relative to control patients, one-sided Wilcoxon rank-sum test, p-value < 2.2×10−16) (Liang et al., 2008).”
From Selective Neuronal Vulnerability in Alzheimer’s Disease: A Network-Based Analysis (2020) · cites this paper as Liang et al., 2008
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 [43]
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- Authors
- Liang, W. S., Dunckley, T., Beach, T. G., Grover, A., Mastroeni, D., Ramsey, K., Caselli, R. J., Kukull, W. A., McKeel, D., Morris, J. C., Hulette, C. M., Schmechel, D., Reiman, E. M., Rogers, J., & Stephan, D. A.
- Affiliations
- Translational Genomics Research Institute (US)
- Banner Sun Health Research Institute (US)
- Mayo Clinic (US)
- National Alzheimer's Coordinating Center (US)
- Washington University in St. Louis (US)
- Duke University (US)
- ORCID
- Venue
- Physiological Genomics
- Publisher
- American Physiological Society
- Published
- 2008-04
- Volume
- 33
- Issue
- 2
- Pages
- 240-256
- ISSN
- 1094-8341 (ISSN-L)
- 1531-2267
- PMC
- PMC2826117
- OpenAlex
- W2097632269
- Cited by
- 309
- References
- 153
- Citations by year
- 2026: 16 · 2025: 15 · 2024: 27 · 2023: 13 · 2022: 17 · 2021: 17 · 2020: 23 · 2019: 19 · 2018: 12 · 2017: 18 · 2016: 9 · 2015: 29 · 2014: 11 · 2013: 15 · 2012: 23
- FWCI
- 10.16
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Physiological Genomics (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (1k01ag024079-01a2)
- National Institute on Aging (AGO7367, P30-AG-19610, AG05 128, R01AG023193, U01AG016976, K01-AG-024079, P50AG005128, 1-R01-AG-023193, P 50 AG05681, P50AG005681, P30AG019610, P01 AG0 3991, P01AG003991)
- National Institute of Neurological Disorders and Stroke (U24NS051872)
- 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, neuronal gene expression, regional brain differences, postmortem brain, laser capture microdissection, entorhinal cortex, hippocampus, posterior cingulate cortex, superior frontal gyrus, primary visual cortex, middle temporal gyrus, amyloid plaques, neurofibrillary tangles
- MeSH terms
- Aged, Alzheimer Disease, Brain, Gene Expression Regulation, Humans, Neurons, Organ Specificity, Protein Kinases, Reproducibility of Results, Amyloid beta-Protein Precursor, Neurofibrillary Tangles, Molecular Chaperones, Reverse Transcriptase Polymerase Chain Reaction, Gene Expression Profiling, Databases, Genetic, Plaque, Amyloid
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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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