Lipofuscin pigment appears very early in life. It has been observed by some scientists in fetal nerve cells, though others have not found it in children under 10. In the cerebral cortex of rats, Dr. Kenneth R. Brizzee and his co-workers found a ten-fold increase in the amount of pigment in aged rats compared to that in young adults. In humans, lipofuscin may accumulate in neurons up to 70 percent of cellular volume before killing them. Figure 1 shows the progressive deterioration of brain cells getting clogged with lipofuscin age pigment. The pigment accumulates at the apex of the nerve cell, blocking the flow of vital nutrients to the long processes extending from the apex. Eventually, the fine nerve cell fibers die, followed by the death of the nerve cell itself. Without the fine interconnecting fibers, nerve cells cannot communicate with each other. Mental functions deteriorate. Figure 2 shows how the lipofuscin content of cells in a particular area of the
human brain builds up over the years.
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Reprinted from Aging, Vol. 1 (Clinical, Morphologic, and Neuro-chemical Aspects in the
Aging Nervous System), H. Brody, D. Harman, and J. Mark Ordy, editors. Copyright ©
1975 by Raven Press Books, Ltd.
Similar to but not identical with lipofuscin, the age pigment ceroid is commonly found in vitamin E-deficient animals. In humans, ceroid is reportedly associated with liver and intestinal diseases which impair vitamin E absorption and utilization. In laboratory mammals, ceroid deposits can accumulate rapidly, becoming visible in only a few days to months under appropriate conditions.
Figure 2. Graph of mean lipofuscin content plotted against age for nerve cells of
inferior olivary nucleus of 67 human cases of age range 11 days to 91 years.
Yet another accumulated pigment, amyloid, is found in the nervous tissue of patients with various disease conditions and in old age. Whereas lipofuscin is composed of lipids (50 percent), proteins (30 percent), and residues, amyloid is made of perhaps three different proteins, including, in one type of amyloid, the immunological proteins from an autoimmune attack. It is thought that amyloid damages nervous tissues by compression and infiltration, blocking cytoplasmic flow and interfering with diffusion, movement, and reaction of vital biochemicals within the cell.
The accumulation of these aging pigments can be prevented or slowed by some prescription drugs. Drs. G. H. Bourne and Kalidas Nandy found that lipofuscin can be removed from cells by a drug called centrophenoxine or meclofenoxate (trade name, Lucidril®), used widely in several European countries. The molecule is made up of dimethylaminoethanol attached to p-chlorophenoxyacetic acid. The former compound is in Deaner®, and is closely related to the diethylaminoethanol in GH-3. The latter compound is half of auxin, a plantgrowth hormone. In spider monkeys, centrophenoxine greatly reduced lipofuscin from brain cells but did not reduce it in the heart or other organs. It also decreased this pigment in the nerve cells of guinea pigs and other rodents. Deaner® (Riker) is the p-acetamidobenzoate salt of dimethylaminoethanol and has many effects similar to those of centrophenoxine.
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