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1. Alzheimer’s disease-specific transcriptomic and epigenomic changes in the tryptophan catabolic pathway

Author

Choe, Kyonghwan, Ali, Muhammad, Lardenoije, Roy, Riemens, Renzo J.M., Pishva, Ehsan, Bickel, Horst, Weyerer, Siegfried, Hoffmann, Per, Pentzek, Michael, Riedel-Heller, Steffi, Wiese, Birgitt, Scherer, Martin, Wagner, Michael, Mastroeni, Diego, Coleman, Paul D., Ramirez, Alfredo, Ramakers, Inez H.G.B., Verhey, Frans R.J., Rutten, Bart P.F., Kenis, Gunter, and van den Hove, Daniel L.A.

Published
2024
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4. Nuclear but not mitochondrial‐encoded oxidative phosphorylation genes are altered in aging, mild cognitive impairment, and Alzheimer's disease

Author

Mastroeni, Diego, Khdour, Omar M, Delvaux, Elaine, Nolz, Jennifer, Olsen, Gary, Berchtold, Nicole, Cotman, Carl, Hecht, Sidney M, and Coleman, Paul D

Subjects
Biomedical and Clinical Sciences, Biological Psychology, Clinical Sciences, Neurosciences, Psychology, Dementia, Neurodegenerative, Brain Disorders, Alzheimer's Disease, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Acquired Cognitive Impairment, Genetics, Aging, 2.1 Biological and endogenous factors, Aetiology, Neurological, Adult, Aged, 80 and over, Alzheimer Disease, Autopsy, Cognition Disorders, Female, Hippocampus, Humans, Male, Mitochondria, Oligonucleotide Array Sequence Analysis, Oxidative Phosphorylation, Alzheimer's disease, Microarray, Mild cognitively impaired, Oxidative phosphorylation-related genes expression, Postmortem brains, Geriatrics, Clinical sciences, Biological psychology
Abstract

IntroductionWe have comprehensively described the expression profiles of mitochondrial DNA and nuclear DNA genes that encode subunits of the respiratory oxidative phosphorylation (OXPHOS) complexes (I-V) in the hippocampus from young controls, age matched, mild cognitively impaired (MCI), and Alzheimer's disease (AD) subjects.MethodsHippocampal tissues from 44 non-AD controls (NC), 10 amnestic MCI, and 18 AD cases were analyzed on Affymetrix Hg-U133 plus 2.0 arrays.ResultsThe microarray data revealed significant down regulation in OXPHOS genes in AD, particularly those encoded in the nucleus. In contrast, there was up regulation of the same gene(s) in MCI subjects compared to AD and ND cases. No significant differences were observed in mtDNA genes identified in the array between AD, ND, and MCI subjects except one mt-ND6.DiscussionOur findings suggest that restoration of the expression of nuclear-encoded OXPHOS genes in aging could be a viable strategy for blunting AD progression.

Published
2017

6. A meta-analysis of epigenome-wide association studies in Alzheimer’s disease highlights novel differentially methylated loci across cortex

Author

Smith, Rebecca G., Pishva, Ehsan, Shireby, Gemma, Smith, Adam R., Roubroeks, Janou A. Y., Hannon, Eilis, Wheildon, Gregory, Mastroeni, Diego, Gasparoni, Gilles, Riemenschneider, Matthias, Giese, Armin, Sharp, Andrew J., Schalkwyk, Leonard, Haroutunian, Vahram, Viechtbauer, Wolfgang, van den Hove, Daniel L. A., Weedon, Michael, Brokaw, Danielle, Francis, Paul T., Thomas, Alan J., Love, Seth, Morgan, Kevin, Walter, Jörn, Coleman, Paul D., Bennett, David A., De Jager, Philip L., Mill, Jonathan, and Lunnon, Katie

Published
2021
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11. Extensive innate immune gene activation accompanies brain aging, increasing vulnerability to cognitive decline and neurodegeneration: a microarray study

Author

Cribbs, David H, Berchtold, Nicole C, Perreau, Victoria, Coleman, Paul D, Rogers, Joseph, Tenner, Andrea J, and Cotman, Carl W

Abstract

AbstractBackgroundThis study undertakes a systematic and comprehensive analysis of brain gene expression profiles of immune/inflammation-related genes in aging and Alzheimer’s disease (AD).MethodsIn a well-powered microarray study of young (20 to 59 years), aged (60 to 99 years), and AD (74 to 95 years) cases, gene responses were assessed in the hippocampus, entorhinal cortex, superior frontal gyrus, and post-central gyrus.ResultsSeveral novel concepts emerge. First, immune/inflammation-related genes showed major changes in gene expression over the course of cognitively normal aging, with the extent of gene response far greater in aging than in AD. Of the 759 immune-related probesets interrogated on the microarray, approximately 40% were significantly altered in the SFG, PCG and HC with increasing age, with the majority upregulated (64 to 86%). In contrast, far fewer immune/inflammation genes were significantly changed in the transition to AD (approximately 6% of immune-related probesets), with gene responses primarily restricted to the SFG and HC. Second, relatively few significant changes in immune/inflammation genes were detected in the EC either in aging or AD, although many genes in the EC showed similar trends in responses as in the other brain regions. Third, immune/inflammation genes undergo gender-specific patterns of response in aging and AD, with the most pronounced differences emerging in aging. Finally, there was widespread upregulation of genes reflecting activation of microglia and perivascular macrophages in the aging brain, coupled with a downregulation of select factors (TOLLIP, fractalkine) that when present curtail microglial/macrophage activation. Notably, essentially all pathways of the innate immune system were upregulated in aging, including numerous complement components, genes involved in toll-like receptor signaling and inflammasome signaling, as well as genes coding for immunoglobulin (Fc) receptors and human leukocyte antigens I and II.ConclusionsUnexpectedly, the extent of innate immune gene upregulation in AD was modest relative to the robust response apparent in the aged brain, consistent with the emerging idea of a critical involvement of inflammation in the earliest stages, perhaps even in the preclinical stage, of AD. Ultimately, our data suggest that an important strategy to maintain cognitive health and resilience involves reducing chronic innate immune activation that should be initiated in late midlife.

Published
2012

15. Alzheimer’s disease-associated (hydroxy)methylomic changes in the brain and blood

Author

Lardenoije, Roy, Roubroeks, Janou A. Y., Pishva, Ehsan, Leber, Markus, Wagner, Holger, Iatrou, Artemis, Smith, Adam R., Smith, Rebecca G., Eijssen, Lars M. T., Kleineidam, Luca, Kawalia, Amit, Hoffmann, Per, Luck, Tobias, Riedel-Heller, Steffi, Jessen, Frank, Maier, Wolfgang, Wagner, Michael, Hurlemann, René, Kenis, Gunter, Ali, Muhammad, del Sol, Antonio, Mastroeni, Diego, Delvaux, Elaine, Coleman, Paul D., Mill, Jonathan, Rutten, Bart P. F., Lunnon, Katie, Ramirez, Alfredo, and van den Hove, Daniël L. A.

Published
2019
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23. Blood RNA transcripts reveal similar and differential alterations in fundamental cellular processes in Alzheimer's disease and other neurodegenerative diseases.

Author

Huseby, Carol J., Delvaux, Elaine, Brokaw, Danielle L., and Coleman, Paul D.

Abstract

Background: Dysfunctional processes in Alzheimer's disease and other neurodegenerative diseases lead to neural degeneration in the central and peripheral nervous system. Research demonstrates that neurodegeneration of any kind is a systemic disease that may even begin outside of the region vulnerable to the disease. Neurodegenerative diseases are defined by the vulnerabilities and pathology occurring in the regions affected. Method: A random forest machine learning analysis on whole blood transcriptomes from six neurodegenerative diseases generated unbiased disease‐classifying RNA transcripts subsequently subjected to pathway analysis. Results: We report that transcripts of the blood transcriptome selected for each of the neurodegenerative diseases represent fundamental biological cell processes including transcription regulation, degranulation, immune response, protein synthesis, apoptosis, cytoskeletal components, ubiquitylation/proteasome, and mitochondrial complexes that are also affected in the brain and reveal common themes across six neurodegenerative diseases. Conclusion: Neurodegenerative diseases share common dysfunctions in fundamental cellular processes. Identifying regional vulnerabilities will reveal unique disease mechanisms. Highlights: Transcriptomics offer information about dysfunctional processes.Comparing multiple diseases will expose unique malfunctions within diseases.Blood RNA can be used ante mortem to track expression changes in neurodegenerative diseases.Protocol standardization will make public datasets compatible. [ABSTRACT FROM AUTHOR]

Published
2023
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32. Meta-analysis of epigenome-wide association studies in Alzheimer's disease highlights novel differentially methylated loci across cortex

Author

Smith, Rebecca G, Pishva, Ehsan, Shireby, Gemma, Smith, Adam R, Roubroeks, Janou A Y, Hannon, Eilis, Wheildon, Gregory, Mastroeni, Diego, Gasparoni, Gilles, Riemenschneider, Matthias, Giese, Armin, Sharp, Andrew J, Schalkwyk, Leonard, Haroutunian, Vahram, Viechtbauer, Wolfgang, Van Den Hove, Daniel L A, Weedon, Michael, Brokaw, Danielle, Francis, Paul T, Thomas, Alan J, Love, Seth, Morgan, Kevin, Coleman, Paul D, Bennett, David A, De Jager, Philip L, Mill, Jonathan, and Lunnon, Katie

Abstract

Epigenome-wide association studies of Alzheimer’s disease have highlighted neuropathology-associated DNA methylation differences, although existing studies have been limited in sample size and utilized different brain regions. Here, we combine data from six DNA methylomic studies of Alzheimer’s disease (N=1,453 unique individuals) to identify differential methylation associated with Braak stage in different brain regions and across cortex. We identified 236 CpGs in the prefrontal cortex, 95 CpGs in the temporal gyrus and ten CpGs in the entorhinal cortex at Bonferroni significance, with none in the cerebellum. Our cross-cortex meta-analysis (N=1,408 donors) identified 220 CpGs associated with neuropathology, annotated to 121 genes, of which 84 genes had not been previously reported at this significance threshold. We have replicated our findings using two further DNA methylomic datasets consisting of a > 600 further unique donors. The meta-analysis summary statistics are available in our online data resource (www.epigenomicslab.com/ad-meta-analysis/).

Published
2021

35. Intracellular Amyloid-ß Detection from Human Brain Sections Using a Microfluidic Immunoassay in Tandem with MALDI-MS

Author

Villarreal, Jorvani Cruz, Kow, Keegan, Pham, Brian, Egatz-Gomez, Ana, Sandrin, Todd R., Coleman, Paul D., and Ros, Alexandra

Abstract

Alzheimer’s disease (AD) currently affects more than 30 million people worldwide. The lack of understanding of AD’s physiopathology limits the development of therapeutic and diagnostic tools. Soluble amyloid-ß peptide (Aß) oligomers that appear as intermediates along the Aß aggregation into plaques are considered among the main AD neurotoxic species. Although a wealth of data are available about Aß from in vitro and animal models, there is little known about intracellular Aß in human brain cells, mainly due to the lack of technology to assess the intracellular protein content. The elucidation of the Aß species in specific brain cell subpopulations can provide insight into the role of Aß in AD and the neurotoxic mechanism involved. Here, we report a microfluidic immunoassay for in situ mass spectrometry analysis of intracellular Aß species from archived human brain tissue. This approach comprises the selective laser dissection of individual pyramidal cell bodies from tissues, their transfer to the microfluidic platform for sample processing on-chip, and mass spectrometric characterization. As a proof-of-principle, we demonstrate the detection of intracellular Aß species from as few as 20 human brain cells.

Published
2023
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36. Meta-analysis of epigenome-wide association studies in Alzheimer’s disease highlights 220 differentially methylated loci across cortex

Author

Smith, Rebecca G., Pishva, Ehsan, Shireby, Gemma, Smith, Adam R., Roubroeks, Janou A.Y., Hannon, Eilis, Wheildon, Gregory, Mastroeni, Diego, Gasparoni, Gilles, Riemenschneider, Matthias, Giese, Armin, Sharp, Andrew J., Schalkwyk, Leonard, Haroutunian, Vahram, Viechtbauer, Wolfgang, van den Hove, Daniel L.A., Weedon, Michael, Walter, Jörn, Coleman, Paul D., Bennett, David A., Jager, Philip L. De, Mill, Jonathan, and Lunnon, Katie

Abstract

Epigenome-wide association studies of Alzheimer’s disease have highlighted neuropathology-associated DNA methylation differences, although existing studies have been limited in sample size and utilized different brain regions. Here, we combine data from six methylomic studies of Alzheimer’s disease (N=1,453 unique individuals) to identify differential methylation associated with Braak stage in different brain regions and across cortex. At an experiment-wide significance threshold (P

Published
2020
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40. A meta-analysis of epigenome-wide association studies in Alzheimer’s disease highlights novel differentially methylated loci across cortex

Author

Smith, Rebecca G., primary, Pishva, Ehsan, additional, Shireby, Gemma, additional, Smith, Adam R., additional, Roubroeks, Janou A.Y., additional, Hannon, Eilis, additional, Wheildon, Gregory, additional, Mastroeni, Diego, additional, Gasparoni, Gilles, additional, Riemenschneider, Matthias, additional, Giese, Armin, additional, Sharp, Andrew J., additional, Schalkwyk, Leonard, additional, Haroutunian, Vahram, additional, Viechtbauer, Wolfgang, additional, van den Hove, Daniel L.A., additional, Weedon, Michael, additional, Brokaw, Danielle, additional, Francis, Paul T., additional, Thomas, Alan J, additional, Love, Seth, additional, Morgan, Kevin, additional, Walter, Jörn, additional, Coleman, Paul D., additional, Bennett, David A., additional, De Jager, Philip L., additional, Mill, Jonathan, additional, and Lunnon, Katie, additional

Published
2020
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