Effects of medications on plasma amyloid beta (Aβ) 42: Longitudinal data from the VITA cohort
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文摘
In the course of cognitive deterioration leading to Alzheimer’s disease (AD) the increase of amyloid beta (Aβ42) in cerebrospinal fluid or plasma might be an initial event. We previously reported about the associations between concomitant medication and plasma Aβ42 levels in the non-demented population cohort of the Vienna transdanube aging study at baseline. In the present study, the longitudinal influence of insulin, gingko biloba, non-steroidal anti-inflammatory drugs (NSAIDs), oral anti-diabetics (sulfonylurea and biguanides), estrogens, fibrates, and statins on plasma Aβ42 are presented. Associated with medial temporal lobe atrophy (MTA), users of insulin showed significantly increased levels of Aβ42. Long-term users of gingko biloba, independent of their MTA, had significantly decreased plasma Aβ42 and the age-dependent increase of plasma Aβ42 was significantly smaller in long-term gingko biloba treated subjects. The use of fibrates also decreased plasma Aβ42 levels. In multiple testing considering interactions between medications, gender, APOE-ε4 presence and creatinine, insulin long-term users again showed significantly increased levels; fibrate and gingko biloba users showed a trend to rather decreased plasma Aβ42 levels compared to the non-users (p = 0.05–0.08). Neither statins nor NSAIDs showed a significant effect on plasma Aβ42 in this model. Measuring the effect on cognition, no single medication studied was a significant predictor of conversion to AD or mild cognitive impairment (MCI). Whether the use of gingko biloba might prevent the conversion to MCI or AD needs to be proven in prospective, clinical trials.

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