Glia Alterations

Glial cells are very numerous and in some parts of the brain they outnumber the nerve cells by 10 to 1. The well-known classification of this type of cells into astrocytes, oligodendrocytes, and microglia in addition to referring to their morphological features also categorizes their specific functions that include providing structural support for nerve cells, isolation and grouping of nerve fibers and terminals, participating in metabolic pathways that modulate the ions, transmitters, and metabolites involved in nerve cell functions. The function of oligodendrocytes is to form the myelin around axons in the CNS; microglia are small cells scattered throughout the nervous system that play a central role in injury and degeneration; that is, these cells proliferate, move to the site where damage has occurred, and transform into large macrophages that remove and phagocytize the debris, thus defending the CNS against inflammation and infection. Glial cells and neurons interact intensely; thus many alterations of this type of cells occurring with advancing age may be secondary to neuronal damage and not regarded as primary glial changes. Given the many functions in which glial cells are involved, it appears difficult to rule out the early different changes affecting these cells in aging. An improved characterization of primary glial changes occurring in the aging CNS has been achieved by the use of recently developed immuno-histochemical and silver impregnation methods that enabled the revelation of new aspects on time-related glial degeneration. As an example, paired helical filaments (PHF), long believed to occur only in neurons, were also demonstrated in astrocytes from AD patients (Nakano et al., 1992). In glial cells, the demonstration of variegated abnormal argyrophilic structures immunoreactive with ant-tau antibodies is supporting the concept that glial cytoskeletal abnormalities are related to the specific pathological condition in which they occur. With specific reference to physiological aging, reactive gliosis, probably occurring as a consequence of neuronal damage, is the most common of all glial changes. It has been found that in the eighth decade there is an age-associated increase in the number of cerebral cortical astrocytes immuno-reactive for glial fibrillary acid protein (GFAP) (Hansen et al., 1987). This reaction is directly connected with the essential function of astrocytes that play important roles both in nutritional supply, via glucose transfer to neurons, and in the metabolism of glutamic acid, used as neurotransmitter. The early step of gliosis is represented by a consistent swelling of the nucleus followed by proliferation of astrocytes and hypertrophy of a strongly GFAP-positive cytoplasm. In the human cerebral cortex, these activated astrocytes are reported to be immunor-eactive for a neurotrophic cytokine (S100^), which is involved in the development of neuritic senile plaques (SP) in AD. In normal aging, S100^-immunoreactive astro-cytes increase in number together with the tissue level of S100£ protein and S100£ mRNA, thus supporting that with advancing age the appearance of SP may predispose to the development of an AD pathological condition (Sheng et al., 1996). Over 60 years, microglia also show changes due to age in the human brain: in addition to an altered morphology, the increased number of activated microglia express the immunomodulatory cytokine interleukin-1, which is paired by increased tissue levels of interleukin-1 mRNA (Mrak et al., 1995), an alteration implicated in AD pathogenesis. On the basis of these data, in addition to the age-related neuronal damage and loss, glial degenerative phenomena also must seriously be taken into account in studying brain aging. A better understanding of glial alterations and of neuron-glia interactions may help in identifying the precocious signs of degenerative phenomena and dysfunction.

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