Abstract
Non-enzymatic glycosylation (NEG) of in vivo proteins is believed to play an important role in the process of senescence. Diabetes mellitus also provides a convenient model to study senescence, as many of its sequalae, e.g. neuropathy, retinopathy, may be found in the post seventy year old normoglycaemic population. Discoveries of the mechanisms by which proteins become irreversibly modified by chronic high levels of glucose and other reducing sugars, has led to an increased understanding of the pathophysiological consequences of senescence. This may eventually enable the development of suitable therapies to improve age-related morbidity.