The prevalence of sleep disturbance in patients with Alzheimer's disease (AD) is common. The purpose of this study is whether quality of sleep (QoS) has effect on quality of life (QoL) in Alzheimer's disease (AD) patients and amnestic mild cognitive impairment (aMCI) patients or not. Method: The participants were included 44 AD patients and 54 aMCI patients in this study. AD patients met NINCDS-ADRDA criteria for "probable" or "possible" AD and K-MMSE score was more than 16, single or multi domain aMCI patients met Peterson's Criteria. The QoS was assessed by Pittsburgh Sleep Quality Index (PSQI) and the QoL by Medical Outcome Study Short From-36 (SF-36). Result: Poor sleep was defined by PSQI score more than 6. Therefore, in AD group 23 patients were good sleepers and 21 patients were poor sleepers and in aMCI group 28 patents were good sleepers and 26 patents were poor sleepers. There was no significant difference in the demographic variables demographic factor and global cognitive function which was assessed by K-MMSE and CDR between good sleeper group and poorer sleep group. The poor sleeper group in AD and aMCI had significantly higher depression score and poorer QoL than good sleeper group. The depression played a role as a mediator between QoS and QoL. Conclusion: QoS was also associated QoL in AD and aMCI and depression seemed to play a role as a mediating variable between QoS and QoL. Therefore, QoS had an effect on QoL indirectly rather than directly. In conclusion, sleep has a great effect on cognitively impaired elder, even in very early stage.

-1-Furan-2-yl-3-pyridin-2-yl-propenone (FPP-3) has recently been synthesized and characterized to have an anti-inflammatory activity through the inhibition of the production of nitric oxide and tumor necrosis factor-α. In the present study, adverse effects of FPP-3 on immune functions were determined in female BALB/c mice. When mice were administered orally with FPP-3 at 125, 250 or 500 mg/kg for 7 consecutive days, FPP-3 suppressed the number of antibody-forming cells and reduced thymus weight at 500 mg/kg. In addition, FPP-3 administered mice exhibited reduced splenic cellularity and numbers of splenocyte subsets, such as CD3 These results suggested that FPP-3 at 500 mg/kg might be immunotoxic, and that FPP-3-induced immunotoxicity might be mediated, at least in part, through the inhibition of cytokine production, such as IL-4.