A fairly clear description of the way aggregates like lipofuscin, which your body cannot break down but nonetheless accumulate through the normal operation of your metabolism, harm your cells: "The most striking morphological change in neurons during normal aging is the accumulation of autophagic vacuoles filled with lipofuscin or neuromelanin pigments. These organelles are similar to those containing the [lipofuscin] associated with neurological disorders, particularly in diseases caused by lysosomal dysfunction. [Lipofuscin and pigments] arise from incompletely degraded proteins and lipids principally derived from the breakdown of mitochondria, or products of oxidized catecholamines. Pigmented autophagic vacuoles may eventually occupy a major portion of the neuronal cell body volume, due to resistance of the pigments to lysosomal degradation and/or inadequate fusion of the vacuoles with lysosomes." As long-lived cells are bloated by vacuoles containing material they can't get rid of, they cease to behave correctly, leading to degeneration and disease. Repairing and preventing this state of affairs requires research like the LysoSENS program, aiming for ways to safely break down lipofuscin and other damaging materials.