Aim: To study the effects of amyloid β(Aβ)1-42/α1-antichymotrypsin (ACT) compound on lipid metabolism of human glioma(DK-MG) cells, and investigate the potential association between disturbed cellular lipid metabolism and pathogenesis of Alzheimer disease (AD). Methods: The experiment was finished in Wallenberg Lab, Malmö Hospital of Lund University from January 2001 to March 2002. Aβ1-42 and ACT were mixed at 10:1 molar ratio and incubated at room temperature for 2 hours, the compound formed Aβ1-42/ACT were studied by using agarose gel electrophoresis and Western blot. The effects of Aβ1-42/ACT on low-density lipoprotein(LDL) uptake, degradation and cholesterol synthesis were evaluated. Intracellular lipid accumulation was assessed with Red Oil O staining, and the expressive levels of mRNA of LDL receptor(LDLr) were assessed with RT-PCR. Results: Western blot analysis using monoclonal antibodies against Aβ1-42 and ACT proved the existence of Aβ1-42/ACT compound. As compared with the cells in the control group, Aβ1-42/ACT significantly increased intracellular lipid accumulation and LDL uptake by 20-fold(t=6.84, P < 0.05) and 50% (t=10.30, P < 0.01), respectively. mRNA expression of LDLr was also increased by 48% (t=20.79, P < 0.01). In contrast, Aβ1-42 or ACT alone had no significant effects on these parameters. None of Aβ1-42, ACT or Aβ1-42/ACT had any effect on LDL degradation and intracellular cholesterol synthesis. Conclusion: The increased contents of intracellular lipid induced by Aβ1-42/ACT compound seems to be a result of increased LDL uptake following the up-regulation of LDLr expression. Disturbed lipid metabolism has been proposed as a pathogenic hypothesis for AD, and the effect of the combination of Aβ1-42 and ACT on cellular lipid metabolism may be related to the pathogenesis of AD.