Matsushima H, Shimohama S, Kawamata J, Fujimoto S, Takenawa T, Kimura J
Department of Neurology, Faculty of Medicine, Kyoto University, Sakyoku, Kyoto 606, Japan.
Int J Mol Med. 1998 Jan;1(1):91-3. doi: 10.3892/ijmm.1.1.91.
The epsilon4 allele of apolipoprotein E (apo E) is increased among patients with sporadic or familial Alzheimer's disease (AD). We examined platelet phospholipase C (PLC)-delta1 activity in AD patients either homozygous for apoepsilon3 or having at least one apo epsilon4 allele. We found that platelet PLC-delta1 activity is reduced from control levels in patients homozygous for apo epsilon3, but not changed in patients with an apo epilson4 allele. Reduced PLC-delta1 activity and apo epsilon3 may contribute to AD pathogenesis apart from the apo epsilon4 allele.
载脂蛋白E(apo E)的ε4等位基因在散发性或家族性阿尔茨海默病(AD)患者中有所增加。我们检测了apoε3纯合子或至少有一个apoε4等位基因的AD患者血小板磷脂酶C(PLC)-δ1的活性。我们发现,apoε3纯合子患者的血小板PLC-δ1活性低于对照水平,但有apoε4等位基因的患者其活性未发生变化。除apoε4等位基因外,PLC-δ1活性降低和apoε3可能也参与了AD的发病机制。