ArticleNeuroscience letters2013
Nicotine promotes survival of cells expressing amyloid precursor protein and presenilin: implication for Alzheimer's disease.
Article in Neuroscience letters, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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Who cites it
4 citing papers in PubMed, 13 citations in OpenAlex.
- Systematic Review of Nicotine Exposure's Effects on Neural Stem and Progenitor Cells.Brain sciences · 2021Review
- Neurotoxicity of e-cigarettes.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2020Review
- Nicotine inhibits the proliferation by upregulation of nitric oxide and increased HDAC1 in mouse neural stem cells.In vitro cellular & developmental biology. Animal · 2014Article
- Cotinine halts the advance of Alzheimer's disease-like pathology and associated depressive-like behavior in Tg6799 mice.Frontiers in aging neuroscience · 2014Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Amyloid-β protein (Aβ) accumulation is one of the major hallmarks of Alzheimer's disease (AD) and plays a crucial role in its pathogenesis. Cellular models whereby amyloid precursor protein (APP) is highly expressed are commonly used to test the efficacy of novel neuroprotective compounds. In addition to Aβ, it is known that mutation in the protein presenilin contributes to early onset AD. Recently, a cellular neuroblastoma model where both APP and presenilin are expressed has become available. Since protective effects of nicotine against various neurotoxins have been observed, this study was designed to determine whether nicotine would also protect against cellular damage induced by APP or APP and presenilin. Wild type neuroblastoma (N2a) cell line, and those transfected with amyloid precursor protein (APP), and the combination of APP and presenilin were pretreated with various concentrations of nicotine and the survivability of the cells were determined by MTT assay. Nicotine dose dependently provided protection against cellular loss in all cell lines, with highest protection in the double transfected (44%) followed by single transfected (30%), and wild type (21%). The effects of nicotine in turn were blocked by mecamylamine, a non-selective nicotinic antagonist. These results suggest differential sensitivity of cell lines representing AD pathology to the protective effects of nicotine and provide further support of therapeutic potential of nicotinic agonists in at least a subtype of AD patients.
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Registered trials
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