ArticleJournal of neurochemistry2009
The purine nucleosides adenosine and guanosine delay axonal degeneration in vitro.
Article in Journal of neurochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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
5 citing papers in PubMed, 6 citations in OpenAlex.
- Critical signaling pathways during Wallerian degeneration of peripheral nerve.Neural regeneration research · 2017Article
- The Guanine-Based Purinergic System: The Tale of An Orphan Neuromodulation.Frontiers in pharmacology · 2016Review
- Enhancement of Peripheral Nerve Regrowth by the Purine Nucleoside Analog and Cell Cycle Inhibitor, Roscovitine.Frontiers in cellular neuroscience · 2016Article
- Purine nucleosides: endogenous neuroprotectants in hypoxic brain.Journal of neurochemistry · 2012Review
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
Axonal degeneration is a key component of many neurodegenerative diseases. Injured axons undergo a program of self-destruction termed Wallerian degeneration that is an active, well-regulated process. The pathways leading to axon fragmentation are uncharacterized, but experiments with wld(s) mutant mice led to the discovery that over-expression of NMN adenylyltransferase 1 or treatment with NAD(+) can inhibit axonal degeneration. In this study, we show that the purine nucleosides adenosine and guanosine, but not inosine, inhibit injury-induced axonal degeneration in cultured dorsal root ganglia neurons. Axons can be preserved by adding adenosine within 6 h of the axonal injury. The presence of adenosine was required continuously after the injury to maintain axonal protection. Together these results suggest that adenosine does not alter the neuronal response to injury, but instead inhibits a local axonal pathway necessary for the commitment and/or execution of the axon destructive program.
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Registered trials
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