LysoSENS plans to target pathogenic AGE crosslinks, a subset of which both trigger and are an effect of type 2 diabetes.
Diabetes is characterized by high blood sugar levels, either due to an inability to produce or an insensitivity to insulin. This high sugar concentration speeds up one of the seven pillar precursors of age-related pathology, advanced glycation endproduct (AGE) crosslinks. AGE crosslinks abnormally bind proteins together with sugar molecules. This impairs protein function, e.g. by stiffening proteins in arteries thus causing high blood pressure. They are normally benign but accumulate increasingly with age as they impair the mechanisms by which they are removed. In sufficient quantity they lead to a cascade of bodily damage, and have been implicated in several age-related pathologies, including atherosclerosis, blindness, hearing loss, and heart disease.
So while we all experience the effects of crosslinks as we get older, diabetics experience these effects faster. By developing enzymes to degrade AGE crosslinks, LysoSENS will aim at the double purpose of inhibiting age-related pathology in the latter third of normal lives and also preventing diabetics from experiencing some aspects of accelerated aging.
In fact, since AGE crosslinks damage the beta cells that produce insulin in the pancreas, they (along with insulin resistance) trigger type 2 diabetes. So AGE crosslinks appear both at the beginning and the end of diabetic pathogenesis, setting up a self-reinforcing loop of damage creation. Development of compounds to break the relevant types of AGE crosslinks may prove an excellent opportunity to break this cycle.
