Genetics of human ageing
Aging is characterised by the accumulation of damage in molecules, cells, and tissues over a lifetime; this frequently reduces an organism's ability to maintain homeostasis under stress conditions and entails a higher risk for many diseases and early mortality. Aging also affects physiological functions.
The intricacy of the process and the significant variation among people and even within tissues within a body make it difficult to identify the elements that control ageing. According to the current understanding of biological ageing, some changes brought on by ageing are planned while others are random and unpredictable. The vast differences in average lifespan among species imply that genotype-specific species differences govern maximum lifespan. The role of a particular genotype on an individual's lifespan can be determined by identifying the genes and mutations that cause progeroid syndromes, which are age-related monogenic hereditary illnesses.
Cell senescence, which results from exposure to both intrinsic and extrinsic ageing factors, is the most noticeable event in an ageing tissue at the cellular level. It is characterised
by a gradual accumulation of DNA damage and epigenetic changes in DNA structure that alter proper gene expression and result in altered cell function.
Genetic and environmental factors influence ageing, which is a complex process. The genotype influences how long a species or an individual will live. One of the main causes of ageing is an exponential rise in the prevalence and mortality rates of cancer and other diseases that are not malignant, as well as gradual tissue atrophy and degeneration brought on by a decline in adult or somatic stem cell function.
Throughout their lifespan, cells are continuously exposed to a hazardous environment. Increased cell damage is a factor in the dysfunction that comes with ageing. The progeroid syndromes, which are brought on by a defect in the systems involved in DNA repair and whose symptoms start early in life, are the finest illustration of DNA damage as a cause of ageing.
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There are numerous genetic causes of ageing. Lifespan is determined by specific gene combinations (genotypes): dramatic differences in duration are seen when a single gene is altered, as in human progeroid disorders. Examples of the significance of genetic factors in ageing include genes that maintain organism structure and function over the course of life, alleles that enhance reproductive potential early in life but have negative effects later in life when their impact has escaped natural selective pressure, and constitutional mutations that are phenotypically relevant until late in life when they have eluded selection and cannot be eliminated from the population. Numerous genetic variations connected to age-related disorders have been discovered through many genome-wide case-control association studies. Examples include the genetic variant linked to Alzheimer's disease in APOE and PCDH11X. (AD).
A number of cellular processes that engage in the process of senescence in an integrated manner make up the complex process of ageing. Future studies will need to ascertain the relative contributions of each of these factors to explain how genetic and epigenetic mechanisms, which are impacted by genes, the environment, and stochastic events, might result in these changes. Although assessments of these long-lived populations have made it possible to identify loci that may be linked to a higher likelihood of living longer, further research is required to confirm these correlations.
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