ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999
Activation of neuronal caspase-3 by intracellular accumulation of wild-type Alzheimer amyloid precursor protein.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 130 citations in OpenAlex.
- Necdin: A purposive integrator of molecular interaction networks for mammalian neuron vitality.Genes to cells : devoted to molecular & cellular mechanisms · 2021Review
- Intake of ω-6 Polyunsaturated Fatty Acid-Rich Vegetable Oils and Risk of Lifestyle Diseases.Advances in nutrition (Bethesda, Md.) · 2020Review
- MicroRNA-338-5p alleviates neuronal apoptosis via directly targeting BCL2L11 in APP/PS1 mice.Aging · 2020Article
- Crashing the computer: apoptosis vs. necroptosis in neuroinflammation.Cell death and differentiation · 2019Review
- Disordered APP metabolism and neurovasculature in trauma and aging: Combined risks for chronic neurodegenerative disorders.Ageing research reviews · 2017Review
- Neuroprotective Effects of Selected Microbial-Derived Phenolic Metabolites and Aroma Compounds from Wine in Human SH-SY5Y Neuroblastoma Cells and Their Putative Mechanisms of Action.Frontiers in nutrition · 2017Article
- Amyloid pore-channel hypothesis: effect of ethanol on aggregation state using frog oocytes for an Alzheimer's disease study.BMB reports · 2015Review
- The construction of common and specific significance subnetworks of Alzheimer's disease from multiple brain regions.BioMed research international · 2015Article
- The multifaceted nature of amyloid precursor protein and its proteolytic fragments: friends and foes.Acta neuropathologica · 2015Review
- PPARα activation attenuates amyloid-β-dependent neurodegeneration by modulating Endo G and AIF translocation.Neurotoxicity research · 2015Article
- The effect of fluorescent nanodiamonds on neuronal survival and morphogenesis.Scientific reports · 2014Article
- Antagonistic interplay between necdin and Bmi1 controls proliferation of neural precursor cells in the embryonic mouse neocortex.PloS one · 2014Article
- Necdin controls proliferation and apoptosis of embryonic neural stem cells in an oxygen tension-dependent manner.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Neuron loss in the 5XFAD mouse model of Alzheimer's disease correlates with intraneuronal Aβ42 accumulation and Caspase-3 activation.Molecular neurodegeneration · 2013Article
- Anti-amyloidogenic and anti-apoptotic role of melatonin in Alzheimer disease.Current neuropharmacology · 2010Article
- Versatile somatic gene transfer for modeling neurodegenerative diseases.Neurotoxicity research · 2009Review
- Apoptosis and in vitro Alzheimer disease neuronal models.Communicative & integrative biology · 2009Article
- Sumoylation of amyloid precursor protein negatively regulates Abeta aggregate levels.Biochemical and biophysical research communications · 2008Article
- Necdin regulates p53 acetylation via Sirtuin1 to modulate DNA damage response in cortical neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Gene expression and biological processes influenced by deletion of Stat3 in pulmonary type II epithelial cells.BMC genomics · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Forced overexpression of wild-type Alzheimer amyloid precursor protein (APP) causes postmitotic neurons to degenerate. Caspase-3 (CPP32) is a principal cell death protease involved in neuronal apoptosis during physiological development and under pathological conditions. Here, we investigated whether APP overexpression activates caspase-3 in human postmitotic neurons using adenovirus-mediated gene transfer. When a recombinant adenovirus vector expressing human wild-type APP695 was infected in vitro into neurally differentiated embryonal carcinoma NT2 cells, only postmitotic neurons underwent severe degeneration. Before neurodegeneration, full-length APP- and Abeta-immunoreactive peptides were accumulated in infected neurons, and caspase-3-like protease activity was markedly elevated. Western blot analysis revealed that activated caspase-3 subunits were generated in APP-accumulating neurons. Such neuronal caspase-3 activation was undetectable in NT2 neurons infected with beta-galactosidase-expressing adenovirus. Addition of the caspase-3 inhibitor acetyl-Asp-Glu-Val-Asp-aldehyde to the culture medium significantly reduced the severity of degeneration exhibited by APP-overexpressing neurons. Immunocytochemical analyses revealed that some APP-accumulating neurons contained activated caspase-3 subunits and exhibited the characteristics of apoptosis, such as chromatin condensation and DNA fragmentation. Activation of caspase-3 was also observed in vivo in rat hippocampal neurons infected with the APP-expressing adenovirus. These results suggest that wild-type APP is an intrinsic activator of caspase-3-mediated death machinery in postmitotic neurons.
Indexed as
Identifiers
10436052PMC6782871W2106630191What 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.