Abstract

The 2014 year ended with celebration: Everolimus, a rapamycin analog, was shown to improve immunity in old humans, heralding "a turning point" in research and new era in human quest for immortality. Yet, this turning point was predicted a decade ago. But what will cause human death, when aging will be abolished?

Highlights

  • In 2003 it was proposed that activation of growthpromoting pathways should cause senescence, when the cell cycle is blocked [58]

  • All gerogenic pathways converge on the mTOR pathway: upstream and downstream [7783]

  • Independently, mTOR pathway was revealed in the studies of human diseases: Parkinson and Alzheimer, cancer and benign tumors, cardiac fibrosis and atherosclerosis, renal hypertrophy and diabetic complications [19, 88,89,90,91,92,93,94,95,96,97]

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Summary

INTRODUCTION

As announced by Lamming et al, “A growing list of side effects make it doubtful that rapamycin would be beneficial in humans.” [14] the same opponent re-invented mTOR-centric model (without appropriate reference), suggesting that “longevity is promoted not via increased insulin sensitivity, but instead via decreased PI3K/Akt/mTOR pathway signaling” [15]. As it was predicted in 2008 [4], opponents take mTOR-centric model for granted. More on that was discussed previously [16, 21,22,23,24,25,26,27]

Genetics of longevity
Cellular senescence
Diseases
Findings
CONCLUSION
Full Text
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