Version 1
: Received: 3 April 2022 / Approved: 7 April 2022 / Online: 7 April 2022 (04:24:23 CEST)
How to cite:
Lissek, T. Activity-Dependent Induction of Younger Molecular, Cellular and Organism Phenotypes. Preprints2022, 2022040055. https://doi.org/10.20944/preprints202204.0055.v1
Lissek, T. Activity-Dependent Induction of Younger Molecular, Cellular and Organism Phenotypes. Preprints 2022, 2022040055. https://doi.org/10.20944/preprints202204.0055.v1
Lissek, T. Activity-Dependent Induction of Younger Molecular, Cellular and Organism Phenotypes. Preprints2022, 2022040055. https://doi.org/10.20944/preprints202204.0055.v1
APA Style
Lissek, T. (2022). Activity-Dependent Induction of Younger Molecular, Cellular and Organism Phenotypes. Preprints. https://doi.org/10.20944/preprints202204.0055.v1
Chicago/Turabian Style
Lissek, T. 2022 "Activity-Dependent Induction of Younger Molecular, Cellular and Organism Phenotypes" Preprints. https://doi.org/10.20944/preprints202204.0055.v1
Abstract
In several mammalian species including humans, complex stimulation patterns such as cognitive challenge and physical exercise lead to improvements in organ function, organism health and performance, as well as possibly longer lifespans. The hypothesis is presented here that activity-dependent transcriptional programs, induced by these environmental stimuli, temporarily and lightly de-differentiate somatic cells such as neurons and muscle cells into a state that resembles functionally younger cells to allow cellular remodeling and adaptation of the organism to environmental change. This cellular adaptation program targets several process classes that are heavily implicated in aging, such as mitochondrial metabolism, cell-cell communication, intracellular signaling and epigenetic information processing and leads to functional improvements in these areas. I reverse engineer these activity-dependent gene programs, identify critical molecular nexus points such as CREB, MEF2 and cFos and speculate as to how one might leverage them to prevent and attenuate human aging-related decline of body function, enhance human performance and restore more youthful levels of function and morphology. The findings presented here can serve as a basis for the study and development of effective longevity efforts as the underlying gene programs could be used as markers for treatment success and as targets for therapy development.
Biology and Life Sciences, Biochemistry and Molecular Biology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.