[Protein-condensation diseases--molecular basis of cataract formation]

There are reasons to classify a number of apparently disparate diseases as "condensation" (or molecular aggregation) diseases. Examples of such condensation diseases include the late phase of diabetes mellitus, Alzheimer's disease and others. With an expanding knowledge, the list of these diseases is likely to increase. We shall describe the underlying common mechanisms, the aim being to find anticataractogenic drugs based on this insight. The common, most important denominator of various clinically differing condensation diseases derives from the interaction of the macromolecules which is in part attractive and in part repulsive. Aggregation resp. clumping of the macromolecules of the crystalline lens, the reasons for light scattering, may be prevented by introducing a number of molecules of various designs into the original macromolecular complex which reduce the tendency of aggregation. Cataract inhibitors of this category may be regarded as effective if they are able to increase the time constant of the normal aging process (i.e. the increment of scatter) by about 20%.