早期研究证明姜黄中主要成分姜黄素可以改善患有类似阿尔茨海默氏症（老年痴呆疾病）那样神经紊乱症状果蝇的活动障碍，进而延长果蝇寿命。相关研究成果已发表在国际权威杂志PLoS One上，在该研究中，研究人员发现姜黄素主要是在疾病的早期阶段，通过抑制对神经元有毒性的纤维状结构以及淀粉样纤维丝状的碎片的形成发挥作用。
从那以后，姜黄素一直被当作能治疗阿尔茨海默病的一种潜在药物来研究。阿尔茨海默氏症的发病过程主要是粘性类淀粉样物质以及牛磺酸蛋白纤维的累积过程。
近日，来自Linkoping大学的研究人员开展的一项研究探究了姜黄素是如何影响转基因果蝇的阿尔茨海默氏症样的神经紊乱症，以此希望能发现姜黄素发挥治疗阿尔茨海默氏症功效的确切靶点。
研究人员共设五组转基因果蝇，这些果蝇都经过基因缺失的方式操作而导致病变。工作人员给予这些苍蝇姜黄素后，结果发现给予姜黄素的果蝇在寿命以及灵活性方面要明显优于那些未接受姜黄素治疗的果蝇要高。
但奇怪的是，研究者并没有在果蝇大脑或是眼睛里观察到淀粉样物质的减少。这一现象表明姜黄素并不能溶解已形成的类淀粉样斑块。值得欣慰的是，姜黄素能减少类淀粉样斑块形成的前体物质的数量，这一前体物质形成减少后，低聚物样的纤维物质形成会大大减少，而这些寡聚体是对大脑神经细胞损害最大的一类有害物质。
研究人员在果蝇动物模型中观察到的姜黄素减少大脑中类淀粉样物质的形成可能就是姜黄素发挥抗阿尔茨海默氏症的作用机理。（生物谷Bioon.com）
doi:10.1371/journal.pone.0031424
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Curcumin Promotes A-beta Fibrillation and Reduces Neurotoxicity in Transgenic Drosophila
Ina Caesar1¤, Maria Jonson1, K. Peter R. Nilsson1, Stefan Thor2, Per Hammarstr?m1*
The pathology of Alzheimer's disease (AD) is characterized by the presence of extracellular deposits of misfolded and aggregated amyloid-β (Aβ) peptide and intraneuronal accumulation of tangles comprised of hyperphosphorylated Tau protein. For several years, the natural compound curcumin has been proposed to be a candidate for enhanced clearance of toxic Aβ amyloid. In this study we have studied the potency of feeding curcumin as a drug candidate to alleviate Aβ toxicity in transgenic Drosophila. The longevity as well as the locomotor activity of five different AD model genotypes, measured relative to a control line, showed up to 75% improved lifespan and activity for curcumin fed flies. In contrast to the majority of studies of curcumin effects on amyloid we did not observe any decrease in the amount of Aβ deposition following curcumin treatment. Conformation-dependent spectra from p-FTAA, a luminescent conjugated oligothiophene bound to Aβ deposits in different Drosophila genotypes over time, indicated accelerated pre-fibrillar to fibril conversion of Aβ1–42 in curcumin treated flies. This finding was supported by in vitro fibrillation assays of recombinant Aβ1–42. Our study shows that curcumin promotes amyloid fibril conversion by reducing the pre-fibrillar/oligomeric species of Aβ, resulting in a reduced neurotoxicity in Drosophila.
