English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Background Generations of biogerontologists have repeatedly observed striking variations in lifespans among individual members of genetically identical cohorts from a wide variety of species when aged under apparently identical environments. It is a reasonable assumption that these differences are accompanied by contrasting patterns of healthspan. Recent studies with C. elegans provide strong evidence that these lifespan variations are largely non-heritable (SL Rea et al., Nature Genet37:894, 2005). One can therefore, conclude that they are driven by stochastic events. Methods The frequencies of somatic mutation seem insufficient to explain these variations. They seem likely to be epigenetically based. I have suggested an explanation (GM Martin, Aging Cell 8:761, 2009) that can be viewed as an extension of the antagonistic pleiotropic model of aging proposed by the late George C. Williams (Evolution 11: 398, 1957). In brief, it is proposed that variegated gene expression within families of homologous cells was selected by evolution as an adaptive trait to ensure survival within unpredictable ecologies.

molecular neurodegeneration

Epigenetic gambling &amp; epigenetic drift as potential mechanisms underlying the quasi-stochastic distributions of late life neurodegenerative disorders