Abstract
The prevalence of age-related diseases is in an upward trend due to increased life expectancy in humans. Age-related conditions are among the leading causes of morbidity and death worldwide currently. Therefore, there is an urgent need to find apt interventions that slow down aging and reduce or postpone the incidence of debilitating age-related diseases. This review discusses the efficacy of emerging anti-aging approaches for maintaining better health in old age. There are many anti-aging strategies in development, which include procedures such as augmentation of autophagy, elimination of senescent cells, transfusion of plasma from young blood, intermittent fasting, enhancement of adult neurogenesis, physical exercise, antioxidant intake, and stem cell therapy. Multiple pre-clinical studies suggest that administration of autophagy enhancers, senolytic drugs, plasma from young blood, drugs that enhance neurogenesis and BDNF are promising approaches to sustain normal health during aging and also to postpone age-related neurodegenerative diseases such as Alzheimer’s disease. Stem cell therapy has also shown promise for improving regeneration and function of the aged or Alzheimer’s disease brain. Several of these approaches are awaiting critical appraisal in clinical trials to determine their long-term efficacy and possible adverse effects. On the other hand, procedures such as intermittent fasting, physical exercise, intake of antioxidants such as resveratrol and curcumin have shown considerable promise for improving function in aging, some of which are ready for large-scale clinical trials, as they are non-invasive, and seem to have minimal side effects. In summary, several approaches are at the forefront of becoming mainstream therapies for combating aging and postponing age-related diseases in the coming years.
Highlights
Prazosin VerapamilInhibits mTOR signaling and protein synthesis, activates adenosine monophosphate-activated protein kinase (AMPK) Inhibits mTOR through ATP competition, promotes LC3II and beclin-1 expression Inhibits Akt and mTOR axis components Activates AMPK to inhibit mTOR and promote autophagy to increase Aβ degradation Targets beclin-1 and increases LC3BII and clears α-synuclein Autophagy through mTOR-independent pathway, NPC1, IL-1β Suppression ATP-competitive mTOR (mTORC1 and mTORC2) inhibition ATP-competitive mTOR (mTORC1 and mTORC2) inhibition Dual ATP-competitive mTOR (mTORC1 and mTORC2) and selective PI3KC1a inhibitor Inhibits IP3-mediated Ca2+ signaling, Inhibits Beclin-1 interaction with IP3R–Bcl-2 complex Inhibits mTOR Inhibits caspase 3-mediated Beclin 1 cleavage, Inhibits acetyltransferase EP300 Increased LC3-II Inhibits mTORC1 pathway p53 inhibitor Suppresses Akt/mTOR pathway, Inhibits Oxidative stress Inhibits mitochondrial membrane 44 (TIM44)-superoxide dismutase 2 (SOD2) pathway Increases p-p53 and p-AMPK and decreases Akt/mTOR Blocks calcium channels [202, 207, 208] [202, 209, 210] [211] [212]
The life expectancy of humans has almost doubled in developed countries in the past century
This study suggested that elimination of senescent cells through administration of senolytic drugs is an efficient therapeutic avenue for treating neurodegenerative disorders
Summary
Inhibits mTOR signaling and protein synthesis, activates adenosine monophosphate-activated protein kinase (AMPK) Inhibits mTOR through ATP competition, promotes LC3II and beclin-1 expression Inhibits Akt and mTOR axis components Activates AMPK to inhibit mTOR and promote autophagy to increase Aβ degradation Targets beclin-1 and increases LC3BII and clears α-synuclein Autophagy through mTOR-independent pathway, NPC1, IL-1β Suppression ATP-competitive mTOR (mTORC1 and mTORC2) inhibition ATP-competitive mTOR (mTORC1 and mTORC2) inhibition Dual ATP-competitive mTOR (mTORC1 and mTORC2) and selective PI3KC1a inhibitor Inhibits IP3-mediated Ca2+ signaling, Inhibits Beclin-1 interaction with IP3R–Bcl-2 complex Inhibits mTOR Inhibits caspase 3-mediated Beclin 1 cleavage, Inhibits acetyltransferase EP300 Increased LC3-II Inhibits mTORC1 pathway p53 inhibitor Suppresses Akt/mTOR pathway, Inhibits Oxidative stress Inhibits mitochondrial membrane 44 (TIM44)-superoxide dismutase 2 (SOD2) pathway Increases p-p53 and p-AMPK and decreases Akt/mTOR Blocks calcium channels [202, 207, 208] [202, 209, 210] [211] [212]
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