Elevated expression of interleukin-1 (IL-1 beta), a pro-inflammatory cytoki
ne secreted by activated microglia, is a pathogenic marker of numerous neur
odegenerative processes including Alzheimer's disease (AD). We have charact
erized a link between IL-1 beta and the 68-kDa neurofilament light (NF-L) p
rotein, which is a major component of the neuronal cytoskeleton. Using huma
n brain aggregate cultures, we found that IL-1 beta treatment significantly
increased NF-L expression in primary neurons. Analysis of mRNA levels demo
nstrated elevated NF-L expression within 72 h while imaging of neurons by i
mmunofluorescent staining for NF-L confirmed IL-1 beta -induced NF-L protei
n expression. These observations suggest a potential inflammatory-induced m
echanism for deregulation of an important cytoskeletal protein, NF-L, possi
bly leading to neuronal dysfunction.