Alzheimers disease (AD) is a neurological disorder characterized by plaques and an elevated immune response. Specifically, increased expression of interleukin (IL)-1 and tumour necrosis factor (TNF)-α, has been observed in AD cerebrospinal fluid and temporal brain tissue. Both of these immunomodulators were shown to carry genetic variants that increase the risk of developing AD. Studies have also established the apolipoprotein E (apoE) gene to be a risk factor for AD with η4 carriers having been found to show lower levels of brain apoE. In the present study, treatment of primary rat mixed glial cell cultures with IL-1β induced a significant increase in extracellular apoE protein. In contrast, treatment primary rat astrocyte and mixed glial cell cultures with TNF-α significantly reduced extracellular apoE protein levels. These results are consistent with the notion that elevated cytokine expression directly modulates immunosuppression and indirectly apoE-mediated neuronal remodeling.
Keywords: Apolipoprotein E, Alzheimer's disease, interleukin-1β, tumor necrosis factor-α
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