An association with the epsilon4 allele was evident in this study, but only in cases of severe cognitive impairment.

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. The NF-B pathway is understood to be controlled in an autoregulatory fashion, so expression of IB is thought to provide a means by which B cells modulate this pathway after stimulation with MIP-1␣. Although the idea of NF-B autoregulation is not novel, this is the first report to suggest the regulation of B cell gene expression by MIP-1␣. In addition, we observed the activation of Jun N-terminal kinase (JNK) and p38 mitogenic-activated protein kinase (MAPK), but not extracellular signal-related kinase (ERK) in response to MIP-1␣. Although p38 and NF-B activity were both necessary for B cell migration, IB gene expression was not affected by p38 inhibition, suggesting that p38 is involved in a separate MIP-1␣-mediated signal transduction pathway. 403