Inflammation is profoundly involved in the development of Alzheimer 's disease (AD) and other neurodegenerative diseases.
Excessive release of proinflammatory cytokines by activated microglia surrounding senile plaques might contribute to the neurodegeneration associated with Alzheimer 's disease (AD).
In the present study , we demonstrate in PARP-1 - / - glial cells a loss of several stress-activated transcription factors as well as decreased expression of genes for cytokines and cellular adhesion molecules.
Cellular PARP-1 activity was recovered when the centrifugal sediment was recombined with the supernatant fraction containing cellular ADP-ribose oligomer acceptor proteins.