Nixon Daniel W
Adjunct Clinical Professor of Medicine, Morehouse School of Medicine, 1611 Atlantic Ave, Sullivan's Island, SC 29482, United States.
Curr Alzheimer Res. 2017;14(8):883-893. doi: 10.2174/1567205014666170216152905.
Cancer and Alzheimer's disease (AD) are both associated with aging, but do not often occur together. Obesity is a shared risk factor for both diseases and may be involved in this curious clinical observation. Fat cells produce many active substances, including leptin and adiponectin; leptin has cancer stimulating and AD inhibiting properties, while adiponectin can inhibit cancer but stimulate AD.
To describe the opposing effects of leptin and adiponectin on cancer and AD, to outline signaling pathways involved in these effects and to suggest new research on effective control strategies for both diseases.
A review was conducted to document the inverse cancer/AD relationship and the role of excess body fat as a common risk factor. Previous studies have suggested the involvement of p53, Wnt and other cell signaling pathways in this inverse relationship. The opposing effects of leptin and adiponectin on these signaling pathways in cancer and AD were evaluated.
The inverse cancer/AD relationship is well documented, as is the role of excess body fat, especially central obesity, in increasing risk for both diseases. Leptin and adiponectin have opposing effects in cancer and AD mediated by signaling factors that influence apoptosis, angiogenesis, and other cell growth controls. Wnt and p53 are prominent among these signaling factors.
Opposing effects of leptin and adiponectin, mediated by specific cell signaling pathways, are involved in the inverse cancer/Ad relationship. Future research aimed at modifying the leptin/adiponectin ratio may lead to important treatment and control approaches in both cancer and AD.
癌症和阿尔茨海默病(AD)均与衰老相关,但并不常同时发生。肥胖是这两种疾病的共同风险因素,可能与这一奇特的临床现象有关。脂肪细胞会产生多种活性物质,包括瘦素和脂联素;瘦素有促癌和抑制AD的特性,而脂联素可抑制癌症但会促进AD。
描述瘦素和脂联素对癌症和AD的相反作用,概述这些作用所涉及的信号通路,并提出针对这两种疾病有效控制策略的新研究方向。
进行一项综述,记录癌症与AD的反向关系以及过量体脂作为共同风险因素的作用。先前的研究表明p53、Wnt和其他细胞信号通路参与了这种反向关系。评估了瘦素和脂联素对癌症和AD中这些信号通路的相反作用。
癌症与AD的反向关系以及过量体脂(尤其是中心性肥胖)在增加这两种疾病风险中的作用都有充分记录。瘦素和脂联素通过影响细胞凋亡、血管生成和其他细胞生长调控的信号因子,在癌症和AD中发挥相反作用。Wnt和p53是这些信号因子中较为突出的。
由特定细胞信号通路介导的瘦素和脂联素的相反作用,参与了癌症与AD的反向关系。未来旨在调节瘦素/脂联素比例的研究可能会带来癌症和AD的重要治疗与控制方法。