A valid method of studying age related degenerative pathologies is to study human genetic diseases that appear to accelerate many, though not necessarily all, features of the aging process. Such diseases are described as progeroid syndromes because of their possible relevance to many aspects of aging and age related disease. This article describes the recent progress made at the cellular and molecular levels in understanding the pathogenesis of one of the best characterised of these disorders, Werner's syndrome. These observations are related to some of the less well characterised progeroid syndromes within the context of the cell senescence hypothesis of aging, a theory formulated to explain the aging of regenerative tissue in normal individuals.
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