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Aging is a universal phenomenon. We consider age as a variable all throughout. It is the most accepted yet most complex process that is being dealt with by the scientists worldwide. Many postulates have been laid in order to explain the possible etiology of aging but the definitive evidence still eludes the genius brains.

If a person experiences accelerated aging , it is the result of genetic mutations occurring either during childhood or on attainment of adulthood. The Progeria syndromes like Werner’s syndrome and Hutchinson Gilford syndrome are nothing but the examples of accelerated aging. Werner’s syndrome , though a rare disorder occurs in adults, which is an autosomal recessive disorder. The person, who develops normally till puberty, suddenly starts developing aging symptoms like graying of hair, cataract, muscular atrophy, alopecia, high incidence of neoplastic diseases and diabetes mellitus.

In Hutchinson Gilford syndrome , however, the onset of accelerated aging is much earlier in childhood. Mutations in LMNA gene cause the syndrome. It is a known fact that though normal in infancy, the children typically start showing signs of “failure to thrive” and start appearing aged. They lose fat under the skin and develop alopecia. The aging process makes the arteries vulnerable and the children develop marked anomalies of arteries (arteriosclerosis), thus leading to earlier heart attacks or strokes. This autosomal dominant condition has proved a breakthrough in research of accelerated aging.

Whether it is Down’s syndrome, Werner’s syndrome or Ataxia telangiectasia, not all syndromes constitute all the characteristics of accelerated aging. They are segmental progeroid syndromes, giving valuable information about the normal aging process as well. The most basic aspect of accelerated aging can be said as, the normal degenerative and deteriorative process that acts on the cellular level is speeded up. This process results in premature onset of aging symptoms that may cause early death.


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