Lipofuscin is the name given to a gunk formed of many varied chemical byproducts of metabolism. It accumulates in your cells with age - and cause a great many problems in doing so. In particular, it accumulates in lysosomes, the recycling units of your cells that are tasked with breaking down unwanted chemical and components (the latter in the process called autophagy). Lysosomes in the old are bloated and inefficient, packed to the gills with lipofuscin that cannot be broken down by the enzymes available to your cells. If your lysosomes aren't working well, then the process of autophagy isn't working well, and you can look back into the Fight Aging! archives to see why that is an issue:
You might think of autophagy as a form of self-maintenance for your cells: it is the destruction of damaged and older cellular components such that newly built components can take their place. It is an attractive, intuitive idea that an increased level of autophagy leads to consistantly better function in cells, which in turn leads to longer-lived animals.
I noticed some coverage today on research into the mechanisms by which lipofuscin is formed, which turns out to tie into iron build up and neurodegeneration:
A glitch in the ability to move iron around in cells may underlie a disease known as Type IV mucolipidosis ( ML4 ) and the suite of symptoms - mental retardation, poor vision and diminished motor abilities - that accompany it ... The same deficit also may be involved in aging and neurodegenerative diseases such as Alzheimer's and Parkinson's
To explore the possible role of iron transport in the disease, Xu's group focused on a protein called TRPML1 [that is responsible for ferrying iron out of the lysosome]. A mutation in the gene that produces TRPML1 is known to cause ML4
Further experiments confirmed that when TRPML1 is defective, iron becomes trapped in the lysosome. One result of the buildup is formation of a brownish waste material, lipofuscin, known as the "aging pigment." In skin cells, lipofuscin is the culprit responsible for the dreaded liver spots that appear with increasing age, but in nerve, muscle and other cells, its accumulation has more serious consequences.
"How lipofuscin causes problems in neurons and muscles is not clear, but it's believed that this is garbage that, in time, compromises the normal function of the lysosome," Xu said. "And we know the lysosome is important for all kinds of cell biology, particularly the recycling of intracellular components, so if it's damaged, the cell is going to suffer." Indeed, abnormal accumulation of lipofuscin is associated with a range of disorders including Alzheimer's disease, Parkinson's disease, and macular degeneration (a degenerative disease of the eye) and also contributes to the aging process.
"In a sense we can think of ML4 as really early onset of aging," Xu said.
"If we can somehow manipulate the lysosome iron level, we probably can provide a treatment for the patient," Xu said. "We're not far enough along for those kinds of experiments yet, but now we know enough to work toward that goal."
This is an interesting avenue of research, but it isn't clear whether it could lead to a way to reverse the problem or merely slow it down. Compare that with the bioremediation approach started by Methuselah Foundation-funded researchers. In that line of work, the aim is isolate bacterial enzymes that break down lipofuscin and that can be safely introduced into the body. Using such enzymes would remove the lipofuscin and thereafter keep it at very low levels, too low to cause issues or contribute to age-related disease.