Chapter 14 Dendritic proliferation in the aging brain as a compensatory repair mechanism

Abstract

Publisher Summary This chapter describes the alterations in dendritic extent as potential compensatory responses to age-related neuronal loss in selected brain regions and discusses the apparent breakdown of this compensatory response in Alzheimer's disease and in extreme old age in some brain regions. In considering alterations in dendritic extent as compensatory changes, changes taking place in the surrounding microenvironment of the dendritic trees being considered are also examined in the chapter. Scientists developed a model of two interacting classes of influences on dendritic extent in the aging brain. The loss of neighboring neurons is a proliferative influence in normal aging, at least up to some limit, which seems to be exceeded in very old age in some brain regions. This proliferative influence seems to be deficient in Alzheimer's disease. Partial denervation is a regressive influence in the aged brain, just as it is during earlier periods in the developmental continuum. There are brain regions in which both of these influences are operating. It is suggested that when both influences are operating on the same cell in the normally aging brain, the final effect on the dendritic tree will be a reflection of the net sum of these two influences. The rat cerebellar Purkinje cells represent one example in which there is both neighbor neuron death and an apparent loss of parallel fiber input.