ArticleExperimental brain research2003
A peptide derived from acetylcholinesterase induces neuronal cell death: characterisation of possible mechanisms.
Article in Experimental brain research, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 56 citations in OpenAlex.
- A Novel 14mer Peptide Inhibits Autophagic Flux via Selective Activation of the mTORC1 Signalling Pathway: Implications for Alzheimer's Disease.International journal of molecular sciences · 2024Article
- A Novel Peptide Driving Neurodegeneration Appears Exclusively Linked to the α7 Nicotinic Acetylcholine Receptor.Molecular neurobiology · 2024Article
- A Novel Bioactive Peptide, T14, Selectively Activates mTORC1 Signalling: Therapeutic Implications for Neurodegeneration and Other Rapamycin-Sensitive Applications.International journal of molecular sciences · 2023Article
- Characterization of a Bioactive Peptide T14 in the Human and Rodent Substantia Nigra: Implications for Neurodegenerative Disease.International journal of molecular sciences · 2022Article
- Assessment of Neurodegenerative Changes in Turkeys Fed Diets with Different Proportions of Arginine and Methionine Relative to Lysine.Animals : an open access journal from MDPI · 2022Article
- A novel process driving Alzheimer's disease validated in a mouse model: Therapeutic potential.Alzheimer's & dementia (New York, N. Y.) · 2022Article
- The role of acetylcholinesterase inhibitors such as neostigmine and rivastigmine on chronic pain and cognitive function in aging: A review of recent clinical applications.Alzheimer's & dementia (New York, N. Y.) · 2019Review
- Modulatory Effects of a Novel Cyclized Peptide in Reducing the Expression of Markers Linked to Alzheimer's Disease.Frontiers in neuroscience · 2018Article
- Neuroprotective effects of curcumin against acetamiprid-induced neurotoxicity and oxidative stress in the developing male rat cerebellum: biochemical, histological, and behavioral changes.Environmental science and pollution research international · 2017Article
- A Review on Potential Mechanisms of Terminalia chebula in Alzheimer's Disease.Advances in pharmacological sciences · 2016Review
- Neuronal AChE splice variants and their non-hydrolytic functions: redefining a target of AChE inhibitors?British journal of pharmacology · 2013Review
- Upregulation of alpha7 Nicotinic Receptors by Acetylcholinesterase C-Terminal Peptides.PloS one · 2009Article
- Exploiting regulatory variation to identify genes underlying quantitative resistance to the wheat stem rust pathogen Puccinia graminis f. sp. tritici in barley.TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik · 2008Article
- Acetylcholinesterase readthrough peptide shares sequence similarity to the 28-53 peptide sequence of the acetylcholinesterase adhesion-mediating site and competes for ligand binding in vitro.Journal of molecular neuroscience : MN · 2007Article
- Acetylcholinesterase in Hirschsprung's disease.Pediatric surgery international · 2005Review
- Cellular stress reactions as putative cholinergic links in Alzheimer's disease.Neurochemical researchReview
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acetylcholinesterase (AChE) exhibits functions unrelated to the catalysis of acetylcholine (ACh) in particular during development. Although the underlying mechanism(s) is presently unknown, a candidate peptide fragment (AChE-peptide) has recently been identified, and been shown to induce a continuum of apoptotic and necrotic neuronal cell death in rat hippocampal organotypic cultures. The aim of this study was to trace the cell death pathway initiated by AChE-peptide. Using specific antagonists, it was possible to track a series of cellular events following application of 1 nM AChE-peptide: NMDA receptor activation, opening of the L-type voltage gated calcium channel, activation of calcium/calmodulin kinase II, generation of reactive oxygen species and caspase activation. Pharmacological interception at any stage of this cascade blocked the effect of 1 nM AChE-peptide on neurite retraction. Lactate dehydrogenase (LDH) release, a marker for cell lysis, was unaffected by 1 nM AChE-peptide. In contrast, cell death induced by 1 mM AChE-peptide, monitored as neurite retraction and increased LDH efflux, was not offset by any drug treatment. These data suggest that nanomolar concentrations of AChE-peptide exhibit pathophysiological activity via an apoptotic pathway that could play an important role in neuronal development and neurodegeneration.
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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.