Lipofuscin is an insoluble pigment also known as lipochrome or wear-and-tear pigment.
Lipofuscin is formed from the oxidation of unsaturated fatty acids and is yellow brown in color.
It consists of 30-70% of oxidized proteins and 20-50% of lipids and contains metal cations and sugar residuals.

The mitochondrial-lysosomal axis theory of agingand the protease inhibitor model of aging.
The former focuses on irreparable oxidative damagecaused by oxygen-driven Fenton reactions associated with mitochondrial processes, while the latter espouses inadequate lysosomal proteolysis as a cause of aging. Both theories have significant merit and lend credence to the ‘garbage catastrophe’ theory of aging, which states that the buildup of recalcitrant non-degradable material within the cell eventually leads to cell senescence or inhibited function.

Lipofuscin is one of the important pigments in aging.
It is found in heart muscle, kidney, liver, retina, ganglion cells and nerve cells.
The level of increase of Lipofuscin in the eye causes macular dehydration and also causes Stargardt disease.
In PNS, it causes neurodegenerative disorders such as neuronal ceroid lipofuscinoses and the most common is Batten disease.
In addition to these, other potential causes of lipofuscin are Alzheimer’s disease and Parkinson’s disease.

With aging, cellular proteostasis becomes less effective, hampering degradation of misfolded proteins, which in turn expose their hydrophobic domains and tend to form high-order complexes with other perinuclear/centrosomal-proximal proteins that are prone to aggregate into aggresomes.
Then, upon lysosomal uptake of these aggregates via macroautophagy, highly cross-linked materials such as lipofuscin accumulate within the lysosomes. Thus, although most of intracellular lipofuscin is in the lysosomes, after inhibition of the macroautophagy pathway, lipofuscin can accumulate also in the cytosol.

Calorie restriction, Vitamin E appears to reduce the amount of lipofuscin in the body.

The nootropic drug piracetam appears to significantly reduce accumulation of lipofuscin in the brain tissue of rats.
Other possible therapies are: Centrophenoxine, Acetyl-L-carnitine, Ginkgo biloba¸ Dimethylethanolamine, and
Wet macular degeneration can be treated using selective photothermolysis where a pulsed unfocused laser predominantly heats and kills lipofuscin-rich cells, leaving untouched healthy cells to multiply and fill in the gaps. This ability to selectively target lipofuscin has opened research opportunities in the field of anti-aging medicine.

Ageless Lipofuscin

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