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. 2016 Jul 18;8:173. doi: 10.3389/fnagi.2016.00173

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Copyright © 2016 Scerbak, Vayndorf, Hernandez, McGill and Taylor.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic summary of results. Non-treated wild-type aging C. elegans touch receptor neurons exhibit increased extended outgrowths from the anterior neuron (ALM) soma and increased abnormal ALM soma by late life (day 11 of adulthood). Alaskan berry and fungus treatments impact this neuron aging trajectory by blocking accumulation of ALM aberrations (i.e., blueberry), increasing the incidence of posterior neuron (PLM) aberrations (i.e., lowbush cranberry), or both (i.e., chaga) when compared to age-matched controls. Nevertheless, all three treatments significantly increase lifespan and improve markers of healthspan (i.e., motility and touch response late in life).