- Submit Abstract
This site is part of the Siconnects Division of Sciinov Group
This site is operated by a business or businesses owned by Sciinov Group and all copyright resides with them.
There are many theories of the biological causes of aging, which suggests that many different mechanisms contribute to the aging process.
Kirkwood proposed that the underlying cause is mainly due to the accumulation of random unrepaired molecular damage over time. This eventually leads to cellular defects and tissue dysfunction resulting in increased frailty and age-related diseases.
Our cells possess quality control systems so that molecular damage can be recognized, repaired or removed. However, due to the energy requirements of these systems, somatic maintenance is not 100% efficient. All molecular components are susceptible to damage including DNA, proteins, lipids and organelles. Sources of damage may be intrinsic, such as reactive oxygen species (ROS) and reactive nitrogen species (RNS) or extrinsic such as UV light, irradiation and exposure to toxins.
In terms of aging, exposure to sources of damage over the human lifespan will vary among individuals and may in part explain the heterogeneity in how individuals age.
The rate of accumulation of stress-induced random molecular damage is dependent on the capacity of the antioxidant system and efficiency of repair systems. As these systems are not 100% efficient, cells always contain some unrepaired damage that leads to activation of a stress response and up-regulation of mechanisms to remove the damage or to prevent the cell division. However, these responses also become less efficient with age so that damaged components accumulate leading to cellular defects, which gives rise to tissue dysfunction and aging.
Many studies into the molecular mechanisms of aging have focused on a particular theory such as the accumulation of somatic mutations, DNA damage and repair, telomere shortening, Loss of protein homoeostasis, Molecular chaperones, protein degradation pathways, protein aggregation, mitochondrial damage and dysfunction, Dysregulation of cellular signalling, DNA methylation dynamics and computational modelling.