Glial reaction in aging and Alzheimer's disease

Abstract

It is well‐established that glial cells play an important role during injury and neurodegenerative processes in the central nervous system. In normal aging, no global glia proliferation is found morphologically, but reactive gliosis has been described in specific areas of the limbic system and neocortex that undergo selective neuronal or synaptic degeneration in nondemented elderly persons. In addition, there is an age‐associated increase in the metabolic turnover of cellular proteins, such as glial fibrillary acidic protein, in human brain tissue, even without detectable signs of neurodegeneration. In contrast to the relatively moderate overall glial changes in normal aging, the close association of activated astrocytes and microglial cells with neuritic plaques and cells undergoing neurofibrillary degeneration in Alzheimer's disease (AD), the expression of receptors for complement by glial cells, and the release of soluble cytokines strongly suggest that inflammatory processes may play an important part in the complex pathophysiological interactions that occur in AD. Understanding the role of glia in age‐associated neurodegenerative disorders may provide new insights into the neurobiology of glia‐neuronal interaction and may allow the development of strategies to alter the disease process. This review aims to summarize some of the important aspects of glial cells in aging and dementia. Microsc. Res. Tech. 43:24–28, 1998.