ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
Presenilin-1-dependent transcriptome changes.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 41 citations in OpenAlex.
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- Preservation Analysis on Spatiotemporal Specific Co-expression Networks Suggests the Immunopathogenesis of Alzheimer's Disease.Frontiers in aging neuroscience · 2021Article
- Transcriptional, Behavioral and Biochemical Profiling in the 3xTg-AD Mouse Model Reveals a Specific Signature of Amyloid Deposition and Functional Decline in Alzheimer's Disease.Frontiers in neuroscience · 2020Article
- A Life at the Interface: The 2017 Hower Award Lecture.Pediatric neurology · 2018Article
- Dynamic presenilin 1 and synaptotagmin 1 interaction modulates exocytosis and amyloid β production.Molecular neurodegeneration · 2017Article
- Integrative network analysis of nineteen brain regions identifies molecular signatures and networks underlying selective regional vulnerability to Alzheimer's disease.Genome medicine · 2016Article
- RXR controlled regulatory networks identified in mouse brain counteract deleterious effects of Aβ oligomers.Scientific reports · 2016Article
- Temporal gene profiling of the 5XFAD transgenic mouse model highlights the importance of microglial activation in Alzheimer's disease.Molecular neurodegeneration · 2014Article
- Why our patients (and we) need basic science research.Neurology · 2013Article
- Chopper is prodeath regardless of the effect of p75ICD on sensitivity to oxidative stress.Oxidative medicine and cellular longevity · 2011Article
- Presenilin transgenic mice as models of Alzheimer's disease.Brain structure & function · 2010Review
- Molecular signatures of neurodegeneration in the cortex of PS1/PS2 double knockout mice.Molecular neurodegeneration · 2008Article
- Microarrays and the microscope: balancing throughput with resolution.The Journal of physiology · 2006Review
- Specificity and timing of neocortical transcriptome changes in response to BDNF gene ablation during embryogenesis or adulthood.Molecular psychiatry · 2006Article
- Pathological and physiological functions of presenilins.Molecular neurodegeneration · 2006Article
- Genetics, transcriptomics, and proteomics of Alzheimer's disease.The Journal of clinical psychiatry · 2006Review
- Role of tyrosine phosphorylation in the antioxidant effects of the p75 neurotrophin receptor.Oxidative medicine and cellular longevityArticle
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Familial forms of Alzheimer's disease (FADs) are caused by the expression of mutant presenilin 1 (PS1) or presenilin 2. Using DNA microarrays, we explored the brain transcription profiles of mice with conditional knock-out of PS1 (cKO PS1) in the forebrain. In parallel, we performed a transcription profiling of the hippocampus and frontal cortex of the FAD-linked DeltaE9 mutant transgenic (TG) mice and matched controls [TG mice expressing wild-type human PS1 (hPS1)]. When the TG and cKO datasets were cross-compared, the majority of the 30 common expression alterations were in opposite direction, suggesting that the FAD-linked PS1 variant produces transcriptome changes primarily by gain of aberrant function. Our microarray studies also revealed an unanticipated inverse correlation of transcript levels between the brains of mice that coexpress DeltaE9 hPS1+ amyloid precursor protein (APP)695 Swe and DeltaE9 hPS1 single transgenic mice. The opposite directionality of these changes in transcript levels must be a function of APP and/or APP derivatives.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.