ArticleNeural regeneration research2026
Low-level expression of Cmyc in mature neurons: Maintaining neuronal function and preventing neurodegeneration.
Article in Neural regeneration research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07074782 (Retinal Ganglion Cell Neuroprotection Under Prostaglandin Analogues), which is not on this map. Not yet cited in PubMed.
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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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Retinal Ganglion Cell Neuroprotection Under Prostaglandin Analogues: NEUROPA - a Retrospective Cohort Study
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7 authors.
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Abstract
JOURNAL/nrgr/04.03/01300535-202606000-00067/figure1/v/2026-02-11T151048Z/r/image-tiff Cmyc , a proto-oncogene, is expressed at extremely low levels in mature neurons and is traditionally thought to have no function in these cells. However, recent studies suggest that Cmyc may play a crucial role in maintaining the health and function of mature dopaminergic neurons. This study assessed the role of Cmyc in dopaminergic neurons and its significance in Parkinson's disease. We used a conditional knockout approach to specifically delete Cmyc in substantia nigra dopaminergic neurons of adult mice. Our findings showed that Cmyc deletion led to progressive neuron loss, Parkinson's disease-like symptoms, downregulation of Klotho, and upregulation of senescence-associated inflammatory factors, along with enhanced oxidative stress and nitrated alpha-synuclein accumulation, ultimately causing neuronal death. In vitro experiments confirmed increased senescence in C-MYC knockout cells, which was partially reversible by KLOTHO overexpression. We conclude that low-level Cmyc expression is essential for maintaining the health of mature dopaminergic neurons and preventing neurodegeneration, and suggest the c-Myc/Klotho axis as a potential therapeutic target for age-related neurodegenerative diseases, including Parkinson's disease. Our study introduces a novel mouse model for Parkinson's disease that replicates a condition associated with normal aging, offering a valuable tool for future research into disease mechanisms and therapeutic strategies.
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