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Additional studies suggested that several soluble factors underlie the rejuvenating effects of the young blood. The growth differentiation factor 11 GDF11 is one of the well-characterized factors in the young blood [ 50 ]. Studies using aged mice have shown that GDF11 treatment alone can reverse age-related muscle dysfunction [ 55 ] and cardiac hypertrophy [ 56 , 57 ], and enhance hippocampal neurogenesis, vasculature and markers of neuronal plasticity in the hippocampus and cerebral cortex.

Circulation of blood from young mice into AD mice did not reduce the deposition of beta-amyloid or microglial activation. However, the procedure reversed the loss of synapses and the abnormal expression of many genes involved in critical neuronal signaling pathways in the hippocampus. Furthermore, improvements in spatial working memory and associative memory were observed with repeated intravenous administration of plasma from young healthy mice to AD mice.

These results provided the idea that young plasma has the potential for slowing down the progression of the AD, and clinical trials testing the effect of young plasma in patients with the AD are already underway [ 59 , 60 ]. A human pilot study found that young donor plasma infusion protocols for adults with the AD are safe and feasible though statistically significant improvements in cognition are yet to be detected. To validate the benefits of infusion of plasma collected from younger individuals for treating aged individuals or individuals with AD, careful, placebo-controlled larger clinical trials will be required.

Several issues need to be validated before recommending transfusion of plasma from younger individuals as an approach to combat aging or prevent AD. These include the age-range of younger donors having plasma that mediates beneficial effects upon transfusions into older individuals, an "optimal age" at which transfusion of plasma from younger individuals into elderly individuals would yield significant cognitive enhancement, and the volume or frequency of transfusions required to achieve substantial cognitive improvement without adverse side-effects [ 54 ].

Also, the possible side effects need to be considered, which may include acute lung injury, circulatory overload, and allergic reactions, transmission of infections, febrile nonhemolytic transfusion reactions, red blood cell alloimmunization, and hemolytic transfusion reactions [ 59 ]. There are also ethical challenges to resolve regarding the application of young blood transfusion [ 61 ]. Diet and eating schemes have a significant influence on the pathogenesis of many age-associated diseases, which can be gleaned from both epidemiological and experimental studies [ 62 - 66 ].

Many investigations in animal prototypes have demonstrated that reduced food intake leads to increased lifespan [ 71 ]. The other beneficial effects include improved gut microbiota composition and metabolome [ 72 ], reduced age-related methylation changes in the brain [ 73 ], increased adult neurogenesis [ 74 , 75 ], improved cognitive function [ 76 - 78 ], protection against age-related neurodegenerative disorders such as dementia [ 65 , 79 ].

Recently, many studies have shown that intermittent fasting IF can have similar effects as CR [ 62 , 64 , 80 , 81 ]. Benefits related to cardiovascular health include protection of heart against ischemic injury [ 82 ], reduced body mass index and blood lipids [ 83 ] improved glucose tolerance [ 84 ], and lower incidence of coronary artery disease [ 85 ]. The positive effects of IF on brain health in pre-clinical studies comprised improved cognitive function with reduced oxidative stress during middle age when IF was commenced in young adult age [ 86 ] and delayed occurrence of age-related brain impairments [ 87 ].

Moreover, in models of ischemic stroke, IF modulated forebrain neurogenesis, autophagy, and apoptosis, attenuated inflammasome activity, suppressed detrimental genetic pathways, and improved recovery [ 88 - 90 ]. IF was also found to be efficient for reducing neuroinflammation and preserving cognitive function after lipopolysaccharide administration, an animal model of systemic bacterial infection [ 91 , 92 ]. A recent study showed that IF improves tissue function and the overall health during aging in fruit flies [ 95 ]. This study demonstrated that just one month of a 2-day fedday fasted IF regime at the beginning of adulthood is adequate to extend lifespan.

Additional analysis revealed that IF enhanced resistance to starvation, oxidative and xenobiotic stress with a higher lipid content, which is one of the mechanisms underlying increased longevity. Furthermore, guts of flies that underwent IF displayed a significant reduction in age-related pathologies and improved gut barrier function with reduced relative bacterial abundance. Another study showed that hour fasting enhanced intestinal stem cell function in young and aged mice by inducing a fatty acid oxidation program [ 96 ], which was evident from findings that acute genetic disruption of Cpt1a, the rate-limiting enzyme in fatty acid oxidation, abrogated the positive effect of fasting on stem cells.

How do the various beneficial effects of IF seen in animal studies relate to humans? Many variations of IF exist, the most common plans are defined here. Another eating protocol involving a hour fast, once or twice per week is termed as eat-stop diet. The other schemes of the diet include alternate day fasting and the warrior diet. The warrior diet involves starvation during the day and eating a huge meal feasting at night.

In human studies, protocols and interpretations of IF-mediated weight loss trend varied considerably [ 81 ]. Most human IF studies did not result in significant weight loss or considerable improvements in metabolic biomarkers. Quite a few questions remain to be dealt with regarding the benefits of IF on human health. First, it is unknown whether or not IF is beneficial to commence at all ages or effective in only certain age groups. Second, the benefits of IF for improving cognitive function need to be assessed in both healthy and obese males and females of different ages with various regimens and durations of IF.

For example, a short-term 28 days IF regimen did not show significant effects on body composition, glucose metabolism or cognitive function in healthy lean men [ 97 ]. Third, examining the adverse effects of IF, if any, particularly in individuals with pre-existing health conditions will be important. Fourth, the type of dietary composition which provides maximal benefits with IF needs to be identified. Finally, it will be helpful to examine the potential positive or negative interactions between IF and physical exercise.

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The highest risk factor for developing sporadic late-onset forms of the AD is aging [ 98 ]. The hippocampus is one of the brain regions most severely affected in the AD, which is also a region in the brain containing neural stem cell NSC niches that add new neurons to the hippocampal circuitry throughout life. Within NSC niches, a subclass of slowly dividing cells expressing markers such as glial fibrillary acidic protein GFAP , sex determining region Y-box 2 Sox-2 , brain lipid-binding protein, nestin, vimentin, and Musashi-1 are the NSCs or Type 1 cells [ 99 - ].

When these cells divide, they display asymmetric division to maintain self-renewal as well as generate transit amplifying cells or type 2 cells. They occur in clusters and proliferate actively to produce a pool of doublecortin DCX expressing neuroblasts or Type 3 cells and some glia [ 99 , ]. The neuroblasts differentiate into mature dentate granule cells expressing neuron-specific nuclear antigen NeuN , Prox-1 and calbindin. Newly born granule cells establish afferent connectivity with the axons coming from the entorhinal cortex and efferent connectivity with the CA3 pyramidal neurons.

Although the extent of hippocampal neurogenesis in adult humans has been challenged recently [ ], there is enough credible evidence to support the existence of neurogenesis in the adult and aged human hippocampus. Studies in animal models have shown that hippocampal neurogenesis decreases during aging [ , - ], and the overall decrease is exacerbated in the AD. The precise mechanistic causes underlying age-related decline in neurogenesis are unclear. Persistence of NSCs with increased quiescence and multiple changes in the microenvironment of NSC niches have been observed in rat models [ , , - ].

However, no decline was seen in the expression of multiple genes essential for NSC proliferation and neurogenesis in the dentate gyrus [ ]. Overall, it appears that age-related reductions in stem cell mitogenic factors, microvasculature and cerebral blood flow, and low-grade inflammation influence reduced neurogenesis in aging because increased neurogenesis could be obtained through interventional strategies that upregulate the concentration of NSC mitogenic factors [ , - ] or improve the microvasculature density and diminish inflammation [ 30 ].

A recent study investigated the effect of age on NSCs and neurogenesis in the senescence-accelerated mouse prone 8 SAMP8 strain, which is a non-transgenic short-lived strain that spontaneously develops a pathological profile similar to that of the AD [ 98 ]. SAMP8 mice displayed an accelerated loss of the NSCs that coincided with an enhanced canonical bone morphogenetic protein BMP signaling and increased astroglial differentiation.

Remarkably, blocking the dysregulation of the BMP pathway and its pro-gliogenic effect in vivo by intracranial delivery of the antagonist Noggin restored hippocampal NSC numbers, neurogenesis, and behavior in SAMP8 mice. These results re-enforce the thought that modulation of the local microenvironment of the NSCs counteracts hippocampal dysfunction in pathological aging. Many studies had suggested earlier that normalization of the activity of NSCs and neurogenesis slows down the evolution of AD when such interventions were applied at the early stage of the disease.

The successful stratagems were physical exercise or exposure to the enriched environment [ - ], inhibition of microglial activation [ ], choline supplementation [ ], curcumin treatment [ ] or directed expression of Neurod1 in cycling hippocampal progenitors [ ]. An elegant study published recently, in addition, demonstrated that hippocampal neurogenesis is impaired before the onset of AD pathology [ ].

Interestingly, neither stimulation of hippocampal neurogenesis alone, nor exercise, in the absence of increased hippocampal neurogenesis, improved cognitive function. When the beneficial effects of exercise on hippocampal neurogenesis and BDNF augmentation were mimicked through genetic or pharmacological means, a similar cognitive improvement was seen in AD mice. Furthermore, suppression of hippocampal neurogenesis resulted in worsened cognitive performance and loss of preexisting dentate granule cells. Thus, pharmacological mimetics of exercise capable of enhancing both hippocampal neurogenesis and BDNF appear to be useful for improving cognitive function in the early stages of the AD [ ].

In summary, combined neurogenesis and BDNF boost during adulthood and middle age may postpone aging, and prevent or delay the onset of the AD. In this context, regular or intermittent physical exercise throughout life seems to be the best and an inexpensive and non-invasive approach for continually maintaining higher levels of hippocampal neurogenesis and BDNF to stave off the AD. Pharmacological interventions mimicking physical exercise may also be useful but need rigorous testing in clinical trials for any adverse side effects.

The benefits of regular physical exercise PE for conserving the function of the cardiovascular, musculoskeletal and nervous systems are well known [ - ]. PE boosts blood flow to the working skeletal muscles by up to fold and moderately to the brain; whereas organs such as liver, kidney, and testes encounter diminished blood flow during PE [ ]. Even with the variability in blood flow to different organs, all organs gain from regular PE.

PE attenuates the age-associated waning of maximal oxygen uptake VO 2 max , the production of reactive oxygen species ROS and functional weakening of various organs [ ]. Moreover, PE curbs the age-related deterioration of the cellular housekeeping system such as the proteasome, autophagy, mitophagy, and DNA repair systems, which positively impact multiple organ functions [ ]. PE also leads to increased mitochondrial levels in the brain, heart, liver, and kidney [ , ]. Thus, the PE-induced surge of maximal oxygen uptake aids organ functions including the effectiveness of antioxidant and repair systems and cellular housekeeping activities.

PE enhances immunity and modulates age-related immunosenescence. Immunosenescence is typified by the weakening of the immune system with alterations to innate and adaptive immunity [ - ]. Age-related changes affect the phenotype and function of immune cells, which can interfere with chemotaxis, intracellular killing, and the response of immune cells to pathogens.

Immunosenescence contributes to the development of several age-related diseases including cardiovascular disease, AD, and diabetes in older individuals, and increases the risk for developing autoimmune diseases and chronic infection [ ]. Thus, PE can also prevent age-related diseases through tempering immunosenescence. The effects of PE may also be useful for normalizing immune system function in conditions such as multiple sclerosis [ ].

PE profoundly promotes the brain function in animals and humans. The aging-related cognitive decline epitomizes a critical risk factor for the onset of dementia and is linked with global neurophysiological alterations [ ]. Remarkably, PE delays the age-related cognitive decline. In animal models, PE has been shown to enhance memory and mood function, accompanied with increased neurogenesis, upregulation of multiple neurotrophic factors including BDNF and improved synaptic plasticity in the hippocampus [ - ]. Besides, PE results in secretion of multiple factors from peripheral organs such as skeletal muscle, liver and adipose tissue, which can also influence neuronal function.

A recent study demonstrated that proteins secreted by skeletal muscle cells could upregulate the expression of DCX and beta-III tubulin TuJ-1 , markers of immature neurons [ ], implying that factors secreted by skeletal muscle in response to PE contribute to PE-induced increased neurogenesis.

Thus, regular PE commencing from young or middle age appears to be a necessary lifestyle change for maintaining good health in old age. Since drugs that significantly prevent age-related cognitive decline are yet to be discovered, it is vital to start PE regimen early in life when the neural reserve is still adequate, to completely avoid or at least postpone the cognitive decline. However, the amount of PE required in young or middle age to maintain healthy cognitive function in old age is yet to be ascertained.

Some previous clinical trials of PE showed positive effects on cognitive performance whereas other trials showed minimal or no positive impact. Nonetheless, it is believed that PE programs that are structured, individualized, and continue for longer durations preserve cognitive performance in older adults [ , ]. Indeed, a recent clinical trial suggested that exercising for at least 52 hours over a six months duration is associated with improved cognitive performance in older adults with or without cognitive impairment [ ].

Another study showed that combined physical and cognitive activity improves or maintains cognitive and physical performance in older individuals diagnosed with mild cognitive impairment MCI , especially the amnestic type [ ]. Clinical trials on the effects of various exercises on the prevention of the AD suggested that long-term physical activity with a multicomponent cognitive intervention improves cognitive function in patients with AD [ ]. Overall, the results imply that, after the onset of MCI or early AD, PE intervention alone may not be sufficient but still has the promise to improve function when combined with adequate cognitive activity.

Oxidative stress has a significant influence in the development of many age-related diseases, which include arthritis, diabetes, dementia, stroke, cancer, atherosclerosis, vascular diseases, obesity, osteoporosis, and metabolic syndromes [ - ]. Reactive oxygen species ROS are generated within the biological system to regulate cellular activities such as cell survival, stressor responses, ion channels, and inflammation [ , ].

However, the elevation of ROS is linked to the onset and progression of aging. Particularly, ROS is believed to exacerbate the progression of age-related diseases via oxidative damage and interaction with mitochondria [ , ]. Multiple studies imply that transient or physiological reactive oxygen species ROS generated by nicotinamide adenine dinucleotide phosphate NADPH oxidases operate as a redox signal to restore cellular homeostasis [ ].

Typically, the competence to recreate cellular homeostasis gradually wanes during aging. However, long-lived animals display an ability to re-establish cellular homeostasis, which promotes healthy aging. Therefore, strategies that control NADPH oxidase activity for local and physiological redox signaling are likely to be useful for promoting healthy aging [ ]. Older adults are more susceptible to oxidative stress due to a reduction in the efficiency of their endogenous antioxidant systems [ ].

The heart and brain, with restricted cell renewal rate and excessive amounts of oxygen intake, are especially susceptible to this phenomenon. Typically, an inverse relationship has been observed between plasma antioxidant levels and the onset and progression of several diseases, which include cardiovascular disease [ ], diabetes [ ], and neurological disorders [ ]. Emerging research suggests that natural antioxidants can control the autoxidation by interrupting the propagation of free radicals or by inhibiting the formation of free radicals.

Through such actions, antioxidants reduce oxidative stress, improve immune function, and increase healthy longevity [ ].

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Antioxidants are capable of scavenging the species that initiate the peroxidation, breaking the autoxidative chain reaction, quenching free radicals, and preventing the formation of peroxides [ ]. Therefore, dietary supplementation with antioxidants has received considerable interest in combating aging. This approach is also consistent with the free radical theory of aging [ , ] that lowering the global level of ROS in the body would retard aging, increase lifespan, and prevent and treat aging-associated diseases [ , ].

However, clinical trials with antioxidants in the elderly population have reported inconsistent findings [ ]. Regarding RESV, a clinical trial reported that 4-months of RESV treatment in middle-aged men with metabolic syndrome increased muscle turnover, lipid metabolism, and accumulation of long-chain saturated, monounsaturated, and polyunsaturated free fatty acids, and produced beneficial alterations in gut microbiota [ ]. Another clinical trial showed that incorporation of RESV to standard antihypertensive treatment is efficient for reducing blood pressure to normal levels, without the need for additional antihypertensive drugs [ ].

This study also implied prevention of liver damage with RESV intake, based on lower levels of hepatic enzyme glutamate-pyruvate transaminase in the serum. Additional clinical trials have shown that RESV treatment improved memory performance allied with enhanced functional connectivity between the hippocampus and the medial prefrontal cortex in healthy overweight elderly individuals [ ]. RESV has also been shown to strengthen neurovascular coupling and cognitive performance in type 2 diabetes patients [ ]. CUR was tested in a randomized clinical trial comprising the healthy elderly population.

In this study, improved sustained attention and working memory was observed with acute CUR administration, and enhanced mood and reduced fatigue were seen with a chronic treatment [ ]. Another recent clinical trial reported that daily oral ingestion of a bioavailable and safe form of CUR improves memory performance over 18 months in middle-aged and older non-demented adults [ ].

Moreover, this study suggested that daily oral CUR consumption may lead to less neuropathological accumulation in the amygdala and the hypothalamus [ ]. Thus, based on the results of clinical trials performed, it appears that both RESV and CUR are safe, well-tolerated and beneficial with minimal side effects. Several herbs or other plant products used in Chinese medicine have also been suggested to promote health and longevity [ - ].

Among these, a Chinese herb named Astragalus membranaceus Huangqi has recently been proposed to have robust antiaging activity [ ]. Astragalus membranaceus is a prime healing herb included in many herbal formulations in the practice of conventional Chinese medication to treat a variety of diseases.

It is also marketed as a life-extending tonic for humans in China [ ]. The significant components of Astragalus membranaceus are polysaccharides, flavonoids, and saponins. The components of Astragalus membranaceus has been shown to increase telomerase activity, and mediate antioxidant, anti-inflammatory, immunoregulatory, anticancer, hypolipidemic, anti-hyperglycemic, hepatoprotective, expectorant, and diuretic effects [ ]. An extract of the dried root of Astragalus membranaceus , called TA, has been reported to promote considerable positive effects on the immune system.

Thus, Astragalus membranaceus may be suitable as a dietary supplement for combating vascular aging, brain aging, and cancer. However, rigorous double-blind, placebo-controlled clinical trials will be required to validate the efficacy of this herbal medicine for combating aging or AD.

The efficacy of intracerebral transplantation or peripheral injection of a variety of stem cells including mesenchymal stem cells MSCs , NSCs or glial-restricted progenitors GRPs has been examined in animal models to improve the function of the aging brain. A study by Hattiangady and associates demonstrated that grafting of NSCs or GRPs into the aging hippocampus leads to the stimulation of endogenous NSCs in the subgranular zone and results in increased production of new dentate granule cells [ ].

This study provided the first demonstration that grafting of GRPs or NSCs is an attractive approach for improving neurogenesis in the aging hippocampus. Consistent with these findings, another study showed that implantation of a human NSC cell line CTX0E03 into the ventricles of aged rats is also useful for increasing neurogenesis in the hippocampus [ ]. Collectively, these results suggested that NSC grafting can promote regeneration in the aged brain through stimulation of endogenous neurogenesis.

A long-term study by Shetty and Hattiangady further revealed that the aged hippocampus could support robust engraftment and differentiation of cells derived from NSC grafts [ ]. An interesting finding is that grafted NSCs showed an ability to establish neurogenic niches in non-neurogenic regions of the aged hippocampus. The occurrence of new neurogenic niches was evidenced through the derivation of new, immature neurons from graft-derived cells within graft cores located in the non-neurogenic regions even at three months after grafting.

Sequential labeling with different birth-dating markers further confirmed that the immature neurons found within graft cores were indeed generated from graft-derived cells in the aged hippocampus. This phenomenon is beneficial if these niches can continuously produce new neurons and glia in the grafted hippocampus, as newly generated neurons and glia are expected to improve not only the microenvironment but also the plasticity and function of the aged hippocampus. Overall, these results have significance because the potential application of NSC grafting for treatment of neurodegenerative disorders at early stages of the disease progression and age-related impairments would mostly involve aged persons as recipients.

Even so, further studies are essential to ascertain the functional implications of NSC grafting into the aged hippocampus and whether NSCs from other sources such as human induced pluripotent stem cells hiPSCs or human embryonic stem cells hESCs would exhibit similar behavior. Another study by Zhang and colleagues showed that retardation of aging and lifespan extension could be achieved in middle-aged mice through implantation of hypothalamic NSCs into the aged hypothalamic nucleus exhibiting inflammatory microenvironment [ ].

A few studies have also examined the effects of administration of MSCs in aging models. Transplantation of adipose tissue-derived MSCs AD-MSCs improved locomotor activity and cognitive function in the aged animals, in parallel with the recovery of acetylcholine levels in brain tissues [ ]. These results suggest that grafting of human ADMSCs can restore the physical and cognitive function of aged mice.

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In another study, Cao and colleagues examined the effects of clinical-grade human umbilical cord-derived MSCs on cognitive aging in a mouse model of aging induced by d-galactose [ ]. Mice received intraperitoneal administration of MSCs once weekly for two weeks. Three months after the administration of MSCs, the hippocampal-dependent learning and memory were found to be improved in aged mice, and the synaptic plasticity was enhanced in the CA1 area of the aged hippocampus. Moreover, MSC administration improved dendritic spine density, postsynaptic density, and neurogenesis in the hippocampus.

Overall, this study demonstrated that peripheral administration of umbilical cord-derived MSCs is beneficial for improving the function of the aged brain. Stem cell therapy has been shown to mediate beneficial effects in several other age-related neurodegenerative disease models. First, a study by Blurton-Jones and associates showed that hippocampal NSC transplantation rescued the spatial learning and memory deficits in aged 3xTg-AD mice [ ].

The cognitive function was improved without altering the pathology of the AD. Gain-of-function and loss-of-function studies revealed that the mechanism underlying a better cognitive function involved improved hippocampal synaptic density mediated by BDNF. In a follow-up study, the same research group showed that transplantation of research grade human NSCs is also effective for improving cognitive function in two complementary models of AD [ ].

It appeared that human NSC transplantation improved cognitive function by enhancing endogenous synaptogenesis. However, similar NSC grafting into month-old Tg mice i. However, clinical trials using human tissue-derived stem cells i. In addition to stem cell grafting approach, activation of endogenous cells in some regions of the body has promise for mediating regeneration during aging. In a recent study, Chunhua Zhao and colleagues propose that activation of mesenchymal tissue system may be a key for regeneration during aging [ ].

The authors propose that triple energizer, which is a name used in Chinese medicine, is the largest organ in the body consisting of all functional cells originated from the MSC system during the embryonic development. This concept elaborates the origin, function and the essence of triple-energizer from the perspective of the human organ system.

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The triple-energizer originates from the intraembryonic coelom of the embryo, which is the mesenchymal tissue system composed of functional cells derived from mesodermal stem cells and the microenvironment. This mesenchymal tissue system, closely linked with organs and tissues, plays a vital role in tissue homeostasis and aging. Besides, authors propose that this system is responsible for the proliferation and differentiation of stem cells in the body, the regeneration, and repair of tissues and organs, immunity, and regulation of a molecular network of cell metabolism in the tissue system [ , - ].

There are many anti-aging strategies in development. Some of which have shown considerable promise for slowing down aging or delaying the onset of age-related diseases. From multiple pre-clinical studies, it appears that upregulation of autophagy through autophagy enhancers, elimination of senescent cells using senolytics, transfusion of plasma from young blood, neurogenesis and BDNF enhancement through specific drugs are promising approaches to sustain normal health during aging and also to postpone age-related diseases such as the AD.

However, these approaches will require critical assessment in clinical trials to determine their long-term efficacy and lack of adverse effects on the function of various tissues and organs. On the other hand, approaches such as different types of IF, regular PE, RESV, and CUR treatment are ready for large-scale clinical trials, as they are non-invasive, and seem to have minimal side-effects. Nonetheless, advancement of stem cell therapy for promoting successful brain aging or reversing AD symptoms and pathology would require clinical trials for safety and efficacy using cells derived from hiPSCs or hESCs, as these sources can provide an unlimited number of specific cell types needed for cell therapy in different conditions.

The contents of this article suggest the views of authors and do not represent the views of the Department of Defense, U. National Center for Biotechnology Information , U. Journal List Aging Dis v. Aging Dis. Published online Dec 4.

Aubrey de Grey - Immortality Timeframe

Ashok K. Madhu 1. Leelavathi N. Author information Article notes Copyright and License information Disclaimer. E-mail: ude. This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed. This article has been cited by other articles in PMC. Abstract The prevalence of age-related diseases is in an upward trend due to increased life expectancy in humans. Keywords: Aging, antioxidants, astragalus, autophagy, curcumin, intermittent fasting, neurogenesis, plasma transfusion, physical exercise, resveratrol, senescent cells, senolytics, stem cells, stem cell therapy, telomeres.

Autophagy enhancement for facilitating successful aging Autophagy is a lysosomal disintegration process, which is protective housekeeping machinery to get rid of damaged cell organelles, longstanding misfolded proteins and colonizing pathogens [ 15 , 16 ].

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Table 1 Autophagy Enhancers. Open in a separate window. Senescent cell elimination as an anti-aging therapy Amongst the perpetrators of organismal aging, the function of senescent cells SCs has caught significant interest. Table 2 Senolytic Drugs. Transfusion of plasma from young individuals to promote successful aging A new procedure for limiting or reversing aspects of aging in various organs throughout the body is the transfusion of blood from the young to the aged, as molecules circulating in the young blood can rejuvenate the aging cells and tissues [ 47 - 49 ].

Intermittent fasting as a means to combat aging Diet and eating schemes have a significant influence on the pathogenesis of many age-associated diseases, which can be gleaned from both epidemiological and experimental studies [ 62 - 66 ]. Promise of neurogenesis enhancement for successful aging and preventing AD The highest risk factor for developing sporadic late-onset forms of the AD is aging [ 98 ]. Physical Exercise for Modulating Aging and Preventing Dementia The benefits of regular physical exercise PE for conserving the function of the cardiovascular, musculoskeletal and nervous systems are well known [ - ].

Promising antioxidants and herbals for promoting successful aging Oxidative stress has a significant influence in the development of many age-related diseases, which include arthritis, diabetes, dementia, stroke, cancer, atherosclerosis, vascular diseases, obesity, osteoporosis, and metabolic syndromes [ - ]. Stem cell therapy for promoting healthy brain aging and reversing AD The efficacy of intracerebral transplantation or peripheral injection of a variety of stem cells including mesenchymal stem cells MSCs , NSCs or glial-restricted progenitors GRPs has been examined in animal models to improve the function of the aging brain.

Conclusions There are many anti-aging strategies in development. Anti-senescence compounds: A potential nutraceutical approach to healthy aging. Ageing Res Rev , 46 — Aging Dis , 8 — The Business of Anti-Aging Science. Trends Biotechnol , 35 — The Mitochondrial Basis of Aging. Mol Cell , 61 — Cancer and Aging - the Inflammatory Connection. Aging Dis , 7 — Programmatic features of aging originating in development: aging mechanisms beyond molecular damage? The genetics of ageing. Nature , — Human Ageing Genomic Resources: integrated databases and tools for the biology and genetics of ageing.

Nucleic Acids Res , 41 :D— The effect of fasting or calorie restriction on autophagy induction: A review of the literature. Ageing Res Rev , 47 — Department of Molecular Biology and Genetics. Archived from the original on 12 March Retrieved 21 March Aarhus Universitet. Archived from the original on 21 March Retrieved 15 December List of publications by Dr. Springer Publishing.

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