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The role of astrocytes in Alzheimer's disease

B-amyloid is the primary protein component of neuritic plaques, which are degenerative foci in brains of patients with Alzheimer's disease (AD). The effects of this naturally occurring B-amyloid on the cells of the central nervous system have not been completely understood. The effect of cytokines such as IL-IB, TNF-a, and IFN-y on astrocytic nitric oxide is well documented; however, the effects of fi-amyloid on astrocytes for their cytokine-mediated release of nitric oxide are not established. In the present study astrocytic release of nitric oxide was studied following exposure to B-amyloid peptide (625-35) in combinations with IL-IB, TNF-a or IFN-y. None of the cytokines induced an increase in nitrite levels (nmol/mg protein) in astrocytic cultures by themselves. However, IFN-y combined with IL-IB or TNF-a induced a significant increase in nitrite levels. Although both IL-IB and TNF-a were effective costimulatory factors, the combination of IFN-y and IL-IB was more effective in increasing nitrite levels in cultures than the combination of IFN-y and TNF-a. B25-35 completely blocked the increase in nitrite levels by IFN-y and TNF-a, whereas B25-35 partially blocked the effect of IFN-7 and IL-IB. These findings warrant a further study to determine how the modulatory action of B-amyloid on cytokine-mediated astrocytic release of nitric oxide affects neuronal functions in AD patients. B-amyloid increases the vulnerability of cultured neurons to glutamate-induced excitotoxic damage. Because astrocytes play a key role in uptake of extracellular glutamate and glutamate uptake is ATP dependent, we studied the effect of B25-35 on glutamate and glucose uptake in cultured hippocampal astrocytes following 7 days