Keywords Apolipoprotein E; Alzheimer’s disease; Glia; Inflammation; Lipopolysaccharide; Signal transduction; JNK; ABCA1; Cholesterol; Astrocytes Introduction ApoE expression itself is regulated by
apexbio injury and glial activation. ApoE in the CNS is expressed primarily in glia [10], [11] and [12] and upregulated after injury [13]. ApoE is downregulated in some types of inflammatory responses; for example, activation of macrophages or glial cells by lipopolysaccharide (LPS) results in decreased apoE levels [8], [14] and [15]. ApoE-induced activation of the low-density lipoprotein receptor family in microglia counteracts LPS-induced microglial inflammation [8]. Activation of these receptors signals a decrease in c-Jun N-terminal kinase (JNK) activation in microglia, which was vital to overcome LPS-induced decrease in apoE
expression [8]. These in vitro studies suggested that JNK inhibition alone may be an effective way to increase apoE protein, and this increase in apoE could have anti-inflammatory properties. Thus, our current study aims to further investigate the impact of JNK inhibition on apoE production in the brain.
