What is aging? Biological aging is the way we change over time, generally making us less healthy and closer to dying of old age. Inside our bodies many types of damage occur at the cellular level and over time this damage can accumulate and show itself as a multitude of pathologies. The chemical reactions taking place inside our bodies are collectively called metabolism. More about metabolism - Wiki. More about biological aging - Wiki. Some key biological basics
Damage occurs as a result of normal metabolism in our bodies; this damage accumulates and eventually shows itself as a multitude of pathologies.
Other damage is also caused by exogenous factors such as over-exposure to sunlight. The damage occurring in our bodies as we age can be categorised into seven types; examples of these and the associated pathologies/ diseases are shown in the following table:
Classification of the types of damage occurring in our bodies as we age made by SENS Foundation and associated pathologies/ diseases
Reactive, destructive free radicals and oxidants produced during metabolism, or by exogenous sources, are implicated in all these seven categories by damaging all sorts of cellular components such as DNA, RNA, proteins and lipids. Short video on the actions of free radicals and antioxidants in the body. Reactive oxygen species (ROS) are created by electrons that leak from the electron transport chain and combine with oxygen. Short video introducing the electron transport chain. ROS formation and activity, and our natural defenses @ ROS
More about damage-based theories of aging can be found at senecence.info
More about damage to DNA: DNA mutations and repair
Certain genes have been found to be directly associated with aging in mammals - genes and aging
Hutchinson- Gilford progeria syndrome is an extremely rare disease that brings about a phenotype very similar to premature aging, generally leading to death in teenage years due to myocardial infarction or stroke. At around 18-24 months of age children with HGPS develop symptoms such as growth failure, loss of body fat and hair, aged-looking skin, stiffness of joints, generalised atherosclerosis and heart disease. 90 % of cases have a change from glycine GGC to glycine GGT in codon 608 of the laminA gene. This activates a cryptic splice donor site to produce a dominant negative form of lamin A protein, denoted progerin, which disrupts nuclear membrane and alters transcription. Screening 150 skin biopsies from unaffected individuals by McClintock et al. showed that a similar splicing occurs in vivo at a low level in the skin at all ages.
Introduction to biology - Prof. Robert A. Weinberg