Abstract
Ratanasampil (RNSP) is a traditional Tibetan medicine used for the treatment of stroke and cerebrovascular diseases. Previous discoveries that RNSP can reduce β-amyloid protein levels and increase learning and memory in Alzheimer’s mouse models (Tg2576) led us to investigate whether RNSP can improve cognitive functions in Alzheimer’s patients. In this study, 146 AD patients living in Qinghai province received either one gram or 0.33 gram daily of RNSP for 16 weeks. Placebo patients received Piracetam. Serum Aβ40 and Aβ42 levels were measured at the beginning of the study and after 4 and 16 weeks of treatment. Compared to the same group before treatment, MMSE scores, ADAS-cog scores and ADL scores were significantly improved (p 0.05, p > 0.05). After 16-week treatment, serum TNF-α, IL-1β, IL-6 and Aβ42 levels were significantly decreased (p < 0. 01) in the high-dose RNSP group, whereas no significant differences were found in the low-dose and placebo groups. The Aβ42/Aβ40 ratio was significantly decreased after 4-week and 16-week treatment in the high-dose RNSP group (p < 0. 05, p < 0.01). Furthermore, serum Aβ42 concentrations had a strong positive correlation with TNF-α, IL-1β and IL-6 levels. There were no observable adverse effects in either treatment or control groups. We conclude that further clinical trials of RNSP in Alzheimer disease are warranted.
Highlights
Alzheimer’s disease (AD) is a progressive neurodegenerative disease commonly seen in the elderly population of developed countries [1,2] as well as in China [3]
We found that RNSP decreased serum Aβ42 concentration and the Aβ42/Aβ40 ratio, and reduced the level of several pro-inflammatory factors, including TNF-α, IL-1β and IL-6
Statistical analyzes showed that the demographic characteristics, education levels, average length of patients diagnosed as AD and basal mini-mental state examination (MMSE) scores of all three groups were not significantly different
Summary
Alzheimer’s disease (AD) is a progressive neurodegenerative disease commonly seen in the elderly population of developed countries [1,2] as well as in China [3]. Overproduction of pro-inflammatory cytokines, such as tumor necrosis factor (TNF-α), inter-leukin-1β (IL-1β) and IL-6, triggers pro-inflammatory responses and promotes neuronal cell damage and excessive Aβ deposition. Both Aβ and pro-inflammatory factors are activators of neurotoxic pathways that lead to brain cell dysfunctions and death [6,7,8]. Anti-inflammatory drugs may help to improve brain function in patients with Alzheimer’s disease. Several epidemiological studies have shown that patients on long-term use of non-steroidal anti-inflammatory drugs (NSAIDs) have a lower risk of developing AD than others of the same age group [9]
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