Campbell V A, Gowran A
Department of Physiology and Trinity College Institute of Neuroscience, Trinity College Dublin, Dublin, Ireland.
Br J Pharmacol. 2007 Nov;152(5):655-62. doi: 10.1038/sj.bjp.0707446. Epub 2007 Sep 10.
Alzheimer's disease is an age-related neurodegenerative condition associated with cognitive decline. The pathological hallmarks of the disease are the deposition of beta-amyloid protein and hyperphosphorylation of tau, which evoke neuronal cell death and impair inter-neuronal communication. The disease is also associated with neuroinflammation, excitotoxicity and oxidative stress. In recent years the proclivity of cannabinoids to exert a neuroprotective influence has received substantial interest as a means to mitigate the symptoms of neurodegenerative conditions. In brains obtained from Alzheimer's patients alterations in components of the cannabinoid system have been reported, suggesting that the cannabinoid system either contributes to, or is altered by, the pathophysiology of the disease. Certain cannabinoids can protect neurons from the deleterious effects of beta-amyloid and are capable of reducing tau phosphorylation. The propensity of cannabinoids to reduce beta-amyloid-evoked oxidative stress and neurodegeneration, whilst stimulating neurotrophin expression neurogenesis, are interesting properties that may be beneficial in the treatment of Alzheimer's disease. Delta 9-tetrahydrocannabinol can also inhibit acetylcholinesterase activity and limit amyloidogenesis which may improve cholinergic transmission and delay disease progression. Targeting cannabinoid receptors on microglia may reduce the neuroinflammation that is a feature of Alzheimer's disease, without causing psychoactive effects. Thus, cannabinoids offer a multi-faceted approach for the treatment of Alzheimer's disease by providing neuroprotection and reducing neuroinflammation, whilst simultaneously supporting the brain's intrinsic repair mechanisms by augmenting neurotrophin expression and enhancing neurogenesis. The evidence supporting a potential role for the cannabinoid system as a therapeutic target for the treatment of Alzheimer's disease will be reviewed herewith.
阿尔茨海默病是一种与年龄相关的神经退行性疾病,伴有认知功能下降。该疾病的病理特征是β-淀粉样蛋白沉积和tau蛋白过度磷酸化,这会引发神经元细胞死亡并损害神经元间的通讯。该疾病还与神经炎症、兴奋性毒性和氧化应激有关。近年来,大麻素发挥神经保护作用的倾向作为减轻神经退行性疾病症状的一种手段受到了广泛关注。据报道,在阿尔茨海默病患者的大脑中,大麻素系统的成分发生了改变,这表明大麻素系统要么促成了该疾病的病理生理学,要么被其改变。某些大麻素可以保护神经元免受β-淀粉样蛋白的有害影响,并能够减少tau蛋白磷酸化。大麻素减少β-淀粉样蛋白引发的氧化应激和神经退行性变,同时刺激神经营养因子表达和神经发生的倾向,是可能对阿尔茨海默病治疗有益的有趣特性。Δ9-四氢大麻酚还可以抑制乙酰胆碱酯酶活性并限制淀粉样蛋白生成,这可能改善胆碱能传递并延缓疾病进展。靶向小胶质细胞上的大麻素受体可能会减少阿尔茨海默病的一个特征——神经炎症,而不会产生精神活性作用。因此,大麻素通过提供神经保护和减少神经炎症,同时通过增强神经营养因子表达和促进神经发生来支持大脑的内在修复机制,为阿尔茨海默病的治疗提供了多方面的方法。本文将综述支持大麻素系统作为阿尔茨海默病治疗靶点潜在作用的证据。