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EMERGENCE OF RIFAMPICIN RESISTANCE DURING RIFAMPICIN‐CONTAINING TREATMENT IN ELDERLY PATIENTS WITH PERSISTENT METHICILLIN‐RESISTANT STAPHYLOCOCCUS AUREUS BACTEREMIA

in the control group, but no statistically significant change in either value was found in the two groups. There was a significant difference in TNF-a level changes (Month 6–baseline) between the groups. Changes in ADAS-Jcog scores significantly correlated with changes in TNF-a (correlation coefficient (r) 5 0.38, P 5.04) but not in IL-6 (r 5 0.19) and hs-CRP levels (r 5 0.14). During the study, both groups showed stable fasting plasma glucose and hemoglobin A1c levels. When compared with baseline, fasting immunoreactive insulin levels at Month 6 decreased significantly in the pioglitazone group (from 7.8 3.9 to 5.7 2.4mU/mL, Po.05) but not in the control group (from 6.7 4.8 to 6.5 2.9 mU/mL). It was found that reduction of TNF-a levels after pioglitazone treatment was associated with cognitive improvement. A previous study found that PPARg agonists inhibit Ab production stimulated by inflammatory cytokines. Proinflammatory cytokine TNF-a, which plays a role in immune system to brain communication, contributes to an exacerbation of neurodegeneration by microglial activation. A recent study showed that high serum TNF-a is associated with long-term cognitive decline in communitydwelling subjects with AD. An increase in TNF-a regulates synaptic scaling and results in disease progression in AD. Therefore, treatment to reduce TNF-a levels might provide some therapeutic benefits for AD. Although a number of studies have examined potential mechanisms through which PPARg might act to ameliorate AD pathogenesis and progression, the anti-inflammatory action of PPARg agonists is at least one plausible explanation for the beneficial effect on AD.