Department of Orthopaedic Surgery, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Department of Anatomy, Cell Biology & Physiology, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Curr Osteoporos Rep. 2024 Oct;22(5):483-494. doi: 10.1007/s11914-023-00851-1. Epub 2024 Jan 18.
This comprehensive review discusses the complex relationship between Alzheimer's disease (AD) and osteoporosis, two conditions that are prevalent in the aging population and result in adverse complications on quality of life. The purpose of this review is to succinctly elucidate the many commonalities between the two conditions, including shared pathways, inflammatory and oxidative mechanisms, and hormonal deficiencies.
AD and osteoporosis share many aspects of their respective disease-defining pathophysiology. These commonalities include amyloid beta deposition, the Wnt/β-catenin signaling pathway, and estrogen deficiency. The shared mechanisms and risk factors associated with AD and osteoporosis result in a large percentage of patients that develop both diseases. Previous literature has established that the progression of AD increases the risk of sustaining a fracture. Recent findings demonstrate that the reverse may also be true, suggesting that a fracture early in the life course can predispose one to developing AD due to the activation of these shared mechanisms. The discovery of these commonalities further guides the development of novel therapeutics in which both conditions are targeted. This detailed review delves into the commonalities between AD and osteoporosis to uncover the shared players that bring these two seemingly unrelated conditions together. The discussion throughout this review ultimately posits that the occurrence of fractures and the mechanism behind fracture healing can predispose one to developing AD later on in life, similar to how AD patients are at an increased risk of developing fractures. By focusing on the shared mechanisms between AD and osteoporosis, one can better understand the conditions individually and as a unit, thus informing therapeutic approaches and further research. This review article is part of a series of multiple manuscripts designed to determine the utility of using artificial intelligence for writing scientific reviews.
本综述全面讨论了阿尔茨海默病(AD)和骨质疏松症这两种在老年人群中普遍存在的疾病之间复杂的关系,这两种疾病都会导致生活质量的下降。本文的目的是简明扼要地阐明这两种疾病之间的许多共同点,包括共同的途径、炎症和氧化机制以及激素缺乏。
AD 和骨质疏松症在各自的疾病发病机制中有许多共同之处。这些共同点包括β淀粉样蛋白沉积、Wnt/β-连环蛋白信号通路和雌激素缺乏。AD 和骨质疏松症的共同机制和危险因素导致很大比例的患者同时患有这两种疾病。以前的文献已经确定,AD 的进展会增加骨折的风险。最近的发现表明,情况可能正好相反,这表明在生命早期发生骨折可能会由于这些共同机制的激活而使人更容易患上 AD。这些共同之处的发现进一步指导了针对这两种疾病的新型治疗方法的发展。本详细综述深入探讨了 AD 和骨质疏松症之间的共同之处,以揭示将这两种看似无关的疾病联系在一起的共同参与者。本文讨论的最终观点是,骨折的发生和骨折愈合的机制会使人在以后的生活中更容易患上 AD,这与 AD 患者骨折风险增加的情况类似。通过关注 AD 和骨质疏松症之间的共同机制,可以更好地分别和整体地理解这些疾病,从而为治疗方法和进一步的研究提供信息。本文是一系列旨在确定使用人工智能撰写科学综述的实用性的多篇文章中的一篇。