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This precise number is maintained by allowing each centriole to nucleate only one centriole per cell cycle i. Yet, how the first cell of the embryo, the zygote, obtains two centrioles has remained a mystery in most mammals and insects. The mystery arose because the female gamete oocyte is thought to have no functional centrioles and the male gamete spermatozoon is thought to have only one functional centriole, resulting in a zygote with a single centriole. However, recent studies in fruit flies, beetles, and mammals, including humans, suggest an alternative explanation: spermatozoa have a typical centriole and an atypical centriole.

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The typical centriole has a normal structure but distinct protein composition, whereas the atypical centriole is distinct in both. This has brought to search for drugs or interventions which may act on these mechanisms without the side effects of calorie restriction. In these cases, then, the environment, that is the traditional diet, has allowed to stimulate the molecular mechanisms which can increase life span.

Among the several changes that occur with the aging process, in the last decade Epigenomics has attracted the interest of many researchers. This was mainly due to the fact that epigenetic modifications summarizing, at least in part, the interaction between the individual genetic background and lifestyle characteristics, should be potentially able to capture part of the unexplained susceptibility observed today for complex diseases the so-called missing heritability problem. Starting from the pioneeristic observations that epigenetic modifications affect not only the aging process but also its quality successful aging [ 54 ], EpiGenome-Wide Association Studies identified hundreds of sites spread along the entire genome in which methylation levels change between oldest old and younger subjects.

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In particular, Horwat and co-workers, on the basis of the methylation levels of CpG units, formulated a mathematical model, the so-called epigenetic clock, that showed some important properties [ 55 ]. First, it was able predict the chronological age of a subject starting from the methylation level of several cells and tissues of his body. Second, it represents one of the most accurate biomarker of age also superior to the estimates obtained from the telomere length. Third, using methylation levels of blood and brain tissues from subjects affected by Down syndrome, it showed that an accelerated aging occur in such a syndrome [ 56 ].

Fourth, it was able to predict all-cause mortality also after adjusting for traditional risk factors [ 57 ]. Finally, when it was used to estimate the biological age of several tissues from supercentenarians, it has been demonstrated that brain and muscle represent the youngest tissues of these exceptional individuals [ 58 ]. However, even if the cause-effect relationship between methylation process and aging is still not clear, the potential applications of this discovery are very wide, ranging from detailed monitoring of changes occurring with age within individual systems or organs muscle, brain, etc.

For this and several other reasons, future advances in this field could help the understanding of the complex physiology of aging, lifespan and age-associated diseases. That is, a few subjects can attain longevity because a lucky combination of polymorphisms which allow them to have an efficient metabolism or an efficient response to different stress. Most of the others can attain a similar result by targeting the same pathways with appropriate life style or interventions.

In this context, the importance of epigenetic factors, both as biomarkers of aging and target of interventions will certainly grow in the forthcoming future. Johnson TE. A personal retrospective on the genetics of aging. Genetic analysis of life-span in Caenorhabditis elegans.

Aging can be genetically dissected into component processes using long-lived lines of Caenorhabditis elegans. Three mutants that extend both mean and maximum life span of the nematode, Caenorhabditis elegans, define the age-1 gene. J Gerontol. Gottlieb S, Ruvkun G. Brain IRS2 signaling coordinates life span and nutrient homeostasis. The Fork head transcription factor DAF transduces insulin-like metabolic and longevity signals in C. Kenyon C. The plasticity of aging: insights from long-lived mutants.

Kenyon CJ.

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The genetics of ageing. The variability of the mitochondrial genome in human aging: a key for life and death? Int J Biochem Cell Biol. Skulachev VP. The programmed death phenomena, aging, and the Samurai law of biology. Exp Gerontol. Evidence of genetic enrichment for exceptional survival using a family approach: the Leiden Longevity Study.

The genetic component of human longevity: analysis of the survival advantage of parents and siblings of Italian nonagenarians. Genetic influence on human lifespan and longevity.

Hum Genet. The heritability of human longevity: a population-based study of Danish twin pairs born — Longevity studies in GenomEUtwin. The genetics of human longevity.

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Ann N Y Acad Sci. Sex and age specificity of susceptibility genes modulating survival at old age. Hum Hered. Life-long sustained mortality advantage of siblings of centenarians. Aging Cell. Ziv E, Hu D.

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Ageing Res Rev. Genetic signatures of exceptional longevity in humans. PLoS One. Genome-wide linkage analysis for human longevity: Genetics of Healthy Aging Study. Potential etiologic and functional implications of genome-wide association loci for human diseases and traits.

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Hum Mol Genet. Lack of replication of genetic associations with human longevity. The application of genetics approaches to the study of exceptional longevity in humans: potential and limitations. Immun Ageing.


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Circ Res. The co-occurrence of mtDNA mutations on different oxidative phosphorylation subunits, not detected by haplogroup analysis, affects human longevity and is population specific. Human longevity and variation in DNA damage response and repair: study of the contribution of sub-processes using competitive gene-set analysis. Population-specific association of genes for telomere-associated proteins with longevity in an Italian population.

Evolution in health and medicine Sackler colloquium: Genetic variation in human telomerase is associated with telomere length in Ashkenazi centenarians. Further support to the uncoupling-to-survive theory: the genetic variation of human UCP genes is associated with longevity. Nat Rev Endocrinol. Nat Genet.

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BMC Med Genet. Effect of interleukin-6 polymorphisms on human longevity: a systematic review and meta-analysis. Molecular mechanisms of brain aging and neurodegenerative disorders: lessons from dietary restriction. Trends Neurosci. A systems biology analysis of the unique and overlapping transcriptional responses to caloric restriction and dietary methionine restriction in rats.

The Okinawan diet: health implications of a low-calorie, nutrient-dense, antioxidant-rich dietary pattern low in glycemic load. J Am Coll Nutr.