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首页 » J Alzheimers Dis:大麻中发现可治疗阿尔茨海默氏症的化合物

J Alzheimers Dis:大麻中发现可治疗阿尔茨海默氏症的化合物

来源:生物谷 2014-08-29 20:58

2014年8月29日讯 /生物谷BIOON/--最近,一项研究发现大麻中一种化合物:D-9-四氢大麻酚(THC),可以减缓或阻止阿尔茨海默氏症。利用阿尔茨海默氏病细胞模型,研究人员发现极低剂量的THC能降低β淀粉样蛋白生成,并阻止这种蛋白质的异常聚集。这些低浓度的四氢大麻酚也选择性地增强线粒体的功能,这有助保持一个健康的大脑。相关研究发表在Journal of Alzheimer's Disease杂志上。

四氢大麻酚是一种强力抗氧化剂,具有神经保护特性,但是这是第一次报告证实该化合物直接通过减少β淀粉样蛋白水平,抑制其聚集,增强线粒体功能,影响阿尔茨海默氏症的病理。

淀粉样蛋白β的水平降低意味着有更少的聚集,其可以防止阿耳茨海默氏病的进展。由于THC是一种天然的和相对安全的淀粉样蛋白抑制剂,利用四氢大麻酚或它的类似物,我们可以开发一种有效的治疗药物。

研究人员指出,低剂量四氢大麻酚的治疗效果,似乎克服了四氢大麻酚的毒性和诱发记忆障碍的风险。虽然我们还远未达成共识,但这项研究表明,四氢大麻酚和四氢大麻酚相关的化合物可能具有阿尔茨海默氏病治疗价值。(生物谷Bioon.com)

The Potential Therapeutic Effects of THC on Alzheimer's Disease

Cao C,et al.

The purpose of this study was to investigate the potential therapeutic qualities of Δ9-tetrahydrocannabinol (THC) with respect to slowing or halting the hallmark characteristics of Alzheimer's disease. N2a-variant amyloid-β protein precursor (AβPP) cells were incubated with THC and assayed for amyloid-β (Aβ) levels at the 6-, 24-, and 48-hour time marks. THC was also tested for synergy with caffeine, in respect to the reduction of the Aβ level in N2a/AβPPswe cells. THC was also tested to determine if multiple treatments were beneficial. The MTT assay was performed to test the toxicity of THC. Thioflavin T assays and western blots were performed to test the direct anti-Aβ aggregation significance of THC. Lastly, THC was tested to determine its effects on glycogen synthase kinase-3β (GSK-3β) and related signaling pathways. From the results, we have discovered THC to be effective at lowering Aβ levels in N2a/AβPPswe cells at extremely low concentrations in a dose-dependent manner. However, no additive effect was found by combining caffeine and THC together. We did discover that THC directly interacts with Aβ peptide, thereby inhibiting aggregation. Furthermore, THC was effective at lowering both total GSK-3β levels and phosphorylated GSK-3β in a dose-dependent manner at low concentrations. At the treatment concentrations, no toxicity was observed and the CB1 receptor was not significantly upregulated. Additionally, low doses of THC can enhance mitochondria function and does not inhibit melatonin's enhancement of mitochondria function. These sets of data strongly suggest that THC could be a potential therapeutic treatment option for Alzheimer's disease through multiple functions and pathways.

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