By Morris Rockstein
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Age-related increases in strain-specific antibodies, such as rheumatoid factor in serum of apparently healthy humans, have been demonstrated (Kunkel, 1964). Antinuclear antibodies have been observed with increased incidence in older humans and in 1 5 % of C 5 7 B L / 6 mice (Kunkel, 1964). An increase in thyroid autoantibodies with age was reported by Goodman, jet a_l. (1963) based upon a study of 1,000 individuals including 396 schizophrenics. The question as to whether the production of such antibodies is due to stimulation of the immune mechanism of the mice by microbial agents or is a result of autostimulation of the animals' own immune system has also been studied by using germ-free mice in our laboratory.
Unfortunately, until we know when the isthmo-optic fibers reach the retina and, more importantly, when they normally establish synaptic contact with their target neurons, definitive evidence on this issue will be lacking. Although it seems somewhat implausible, a possible criticism of many of the studies, in which a pattern of neuronal degeneration has been inferred from successive cell counts, is that much of the apparent disappearance of neurons is due to the misidentification, at the earliest stages, of cells which later will become more clearly recognizable as neuroglia.
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