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Scientists speculate that the many losses in function that occur in cells
as they approach senescence (loss of capacity for division) increase their
vulnerability to the diseases or pathologies that are so common in old age.
However, to date, the evidence for this idea exists only in animal models.
Some data from the study of humans does point to at least a theoretical
role for cellular senescence in the diseases of aging.
For example, evidence from research on Werner syndrome, an inherited
disease of premature aging, suggests that cellular senescence can wreak
a range of cellular havoc that can result in age-related diseases. Comparisons
of cells in culture from younger persons with Werner syndrome and older
persons shows that both groups of cells have a limited ability to reproduce
further. Both cell types also go on to form abnormal extracellular matrixes,
the frameworks that hold cells together as tissues. This observation suggests
that a small number of senescent cells can affect neighboring cells and
tissues and perhaps contribute to age-related declines in the function
of those cells and tissues.
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