ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998
Overexpression in neurons of human presenilin-1 or a presenilin-1 familial Alzheimer disease mutant does not enhance apoptosis.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
19 citing papers in PubMed, 103 citations in OpenAlex.
- The endocrine dyscrasia that accompanies menopause and andropause induces aberrant cell cycle signaling that triggers re-entry of post-mitotic neurons into the cell cycle, neurodysfunction, neurodegeneration and cognitive disease.Hormones and behavior · 2015Review
- Critical role of presenilin-dependent γ-secretase activity in DNA damage-induced promyelocytic leukemia protein expression and apoptosis.Cell death and differentiation · 2013Article
- γ-Secretase complexes containing caspase-cleaved presenilin-1 increase intracellular Aβ(42) /Aβ(40) ratio.Journal of cellular and molecular medicine · 2011Article
- Neuropathological changes in brain cortex and hippocampus in a rat model of Alzheimer's disease.Iranian biomedical journal · 2011Article
- Coeloglossum viride var. bracteatum extract protects against amyloid toxicity in rat prefrontal cortex neurons.International journal of clinical and experimental medicine · 2010Article
- Mitochondrial and Cell Death Mechanisms in Neurodegenerative Diseases.Pharmaceuticals (Basel, Switzerland) · 2010Article
- Rab5 mediates an amyloid precursor protein signaling pathway that leads to apoptosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Alterations in presenilin 1 processing by amyloid-beta peptide in the rat retina.Experimental brain research · 2007Article
- Dysfunction of amyloid precursor protein signaling in neurons leads to DNA synthesis and apoptosis.Biochimica et biophysica acta · 2007Review
- Presenilin-dependent gamma-secretase-mediated control of p53-associated cell death in Alzheimer's disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- The gonadotropin connection in Alzheimer's disease.Endocrine · 2005Review
- PS1 activates PI3K thus inhibiting GSK-3 activity and tau overphosphorylation: effects of FAD mutations.The EMBO journal · 2004Article
- DNA synthesis and neuronal apoptosis caused by familial Alzheimer disease mutants of the amyloid precursor protein are mediated by the p21 activated kinase PAK3.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Wild-type and mutated presenilins 2 trigger p53-dependent apoptosis and down-regulate presenilin 1 expression in HEK293 human cells and in murine neurons.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Presenilin-1 P264L knock-in mutation: differential effects on abeta production, amyloid deposition, and neuronal vulnerability.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000Article
- Presenilin-1 regulates the neuronal threshold to excitotoxicity both physiologically and pathologically.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- Apoptotic activities of wild-type and Alzheimer's disease-related mutant presenilins in Drosophila melanogaster.The Journal of cell biology · 1999Article
- Activation of neuronal caspase-3 by intracellular accumulation of wild-type Alzheimer amyloid precursor protein.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
- Mutant presenilin-1 induces apoptosis and downregulates Akt/PKB.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Programmed cell death, or apoptosis, has been implicated in Alzheimer's disease (AD). DNA damage was assessed in primary cortical neurons infected with herpes simplex virus (HSV) vectors expressing the familial Alzheimer's disease (FAD) gene presenilin-1 (PS-1) or an FAD mutant of this gene, A246E. After infection, immunoreactivity for PS-1 was shown to be enhanced in infected cells. The infected cells exhibited no cytotoxicity, as evaluated by trypan blue exclusion and mitochondrial function assays. Quantitative analysis of cells that were immunohistochemically labeled using a Klenow DNA fragmentation assay or the TUNEL method revealed no enhancement of apoptosis in PS-1-infected cells. This result was confirmed using assays for chromatin condensation and for DNA fragmentation. Expression of PS-1 protected against induction of apoptosis in the cortical neurons by etoposide or staurosporine. The specificity of this phenotype was demonstrated by the fact that cortical cultures infected with recombinant HSV vectors expressing the amyloid precursor protein (APP-695) showed, in contrast, a significant increase in the number of apoptotic cells and an increase in DNA fragmentation for all parameters tested. Our results indicate that overexpression of wild-type or A246E mutant PS-1 does not enhance apoptosis in postmitotic cortical cells and suggest that the previously reported enhancement of apoptosis by presenilins may be dependent on cell type.
Indexed as
Identifiers
9822738PMC6793279W2136825556What OpenQuestion holds
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.