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Intervention of Aging -

Intervention of Aging


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A model is suggested which describes how epigenetic regulation of gene transcription by modulation of the chromatin structure in stem cells can account for regulation of the aging program. 


Centrioles - Counter Of Life

...Therefore, ageing factors should be contained in cytoplasm, and if we recall that the age of cells is determined not by the time but by the number of cellular divisions, and the division process is directly connected with centrioles, then centrioles in particular are most logical to be considered the clock measuring cellular life.


Are Telomeres the Key to Aging and Cancer?

Each time a cell divides, the telomeres get shorter. When they get too short, the cell no longer can divide and becomes inactive or "senescent" or dies. This process is associated with aging, cancer and a higher risk of death.


Possible Mitochondrial relationships to aging

Given the role of mitochondria as the cell's powerhouse, there may be some leakage of the high-energy electrons in the respiratory chain to form reactive oxygen species. This can result in significant oxidative stress in the mitochondria with high mutation rates of mitochondrial DNA.[73] A vicious cycle is thought to occur, as oxidative stress leads to mitochondrial DNA mutations, which can lead to enzymatic abnormalities and further oxidative stress. A number of changes occur to mitochondria during the aging process. Tissues from elderly patients show a decrease in enzymatic activity of the proteins of the respiratory chain.[74] Large deletions in the mitochondrial genome can lead to high levels of oxidative stress and neuronal death in Parkinson's disease.[75] Hypothesized links between aging and oxidative stress are not new and were proposed over 50 years ago;[76] however, there is much debate over whether mitochondrial changes are causes of aging or merely characteristics of aging. One notable study in mice demonstrated no increase in reactive oxygen species despite increasing mitochondrial DNA mutations, suggesting that the aging process is not due to oxidative stress.[77] As a result, the exact relationships between mitochondria, oxidative stress, and aging have not yet been settled.

Network Models for Aging

Some of the qualitative views of aging as an accumulation of errors have been incorporated in detailed models for the interactions of normal and defective proteins, free radicals, antioxidants, and the protein production machinery in the cell. These models, given by Kowald & Kirkwood (1994, 1996), Kirkwood & Kowald (1997), have been called the network theory of aging, as they illustrate the network-like interconnections of many components of the system that are required to control cellular homeostasis.



Chaperone proteins may hold clue to aging process

The finding provides direct evidence that a class of proteins plays a role in extending life, because the capacity to moderate stress is a central function to regulating the mechanism of aging.

Molecular Basis of Aging

Asparagine is the amide of aspartic acid. The amide group does not carry a formal charge under any biologically relevant pH conditions. The amide is rather easily hydrolyzed, converting asparagine to aspartic acid. This process is thought to be one of the factors related to the molecular basis of aging.

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