Immune Reactions in Aging Brain and Senile Dementia
The immune system which provides specific defense mechanisms in our body may prove destructive in senescence. Immunologic competence is a growth-related process and may undergo deteriorative changes during aging. Such a self-destructive immunological reaction, often referred to as an autoimmune phenomenon, may give rise to pathological changes and reduction of life expectancy. There is considerable evidence in the literature to indicate that autoimmune reactions occur with increased frequency in the aged (Comfort, 1963). Although controversy exists on the processes underlying these changes, it is generally believed to result from the emergence of new antigenic stimuli or from the loss of acquired immunologic tolerance associated with aging. The autoimmune theory was first proposed by Burnet (1959). He described these changes as being due to the formation of ‘forbidden clones of cells’ arising from the derranged stem cells located in the reticulo-endothelial system, lymph nodes, spleen or bone marrow. Burch (1968), the leading proponent of the autoimmune theory of aging, proposed that several factors acting throughout life may significantly alter the process of acquired immunologic tolerance resulting in the increase of forbidden clones and incidence of autoimmune disorders. Walford (1962, 1967 and 1970), on the other hand, hypothesized that aging may be due to long-term low-grade histo-incompatability reactions among the body’s population of cells resulting in cell death. The possible deterioration of the immune system during aging in mammals has been studied by Makinodan (1976) who suggested that this might be due to either intrinsic changes in T and B cells or their interaction, thus making them less efficient.
KeywordsSenile Plaque Aging Brain Senile Dementia Stumptail Macaque Antineuron Antibody
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