| First Author | Liu L | Year | 2016 |
| Journal | Neuroscience | Volume | 330 |
| Pages | 236-46 | PubMed ID | 27256505 |
| Mgi Jnum | J:236499 | Mgi Id | MGI:5806210 |
| Doi | 10.1016/j.neuroscience.2016.05.050 | Citation | Liu L, et al. (2016) Neuronal expression of ILEI/FAM3C and its reduction in Alzheimer's disease. Neuroscience 330:236-46 |
| abstractText | Decrease in brain amyloid-beta (Abeta) accumulation is a leading strategy for treating Alzheimer's disease (AD). However, the intrinsic mechanism of the regulation of brain Abeta production is largely unknown. Previously, we reported that ILEI (also referred to as FAM3C) binds to the gamma-secretase complex and suppresses Abeta production without inhibiting gamma-secretase activity. In this study, we examined ILEI expression in mouse brain using immunohistochemistry and subcellular fractionation. Brain ILEI showed widespread expression in neurons and ependymal cells but not in glial and vascular endothelial cells. Neuronal ILEI resided in perinuclear vesicular structures, which were positive for a marker protein of the trans-Golgi network. Although ILEI immunostaining was negative at synaptic terminals, synaptosome fractionation analysis suggested that ILEI was enriched in presynaptic terminals, particularly in the active zone-docked synaptic vesicles. ILEI expression levels in brain peaked during the postnatal period and declined with age. In comparison with age-matched control brains, the number of ILEI-immunoreactive neurons decreased in AD brains, although the subcellular localization was unaltered. Our results suggest that a decline of ILEI expression may cause accumulation of Abeta in the brain and the eventual development of AD. |
