Traumatic brain injury (TBI) is a major health problem in the United States, which affects about 1.7 million people each year. Glial cells, T-cells, and mast cells perform specific protective functions in different regions of the brain for the recovery of cognitive and motor functions after central nervous system (CNS) injuries including TBI. Chronic neuroinflammatory responses resulting in neuronal death and the accompanying stress following brain injury predisposes or accelerates the onset and progression of Alzheimer’s disease (AD) in high-risk individuals. About 5.7 million Americans are currently living with AD. Immediately following brain injury, mast cells respond by releasing prestored and preactivated mediators and recruit immune cells to the CNS. Blood-brain barrier (BBB), tight junction and adherens junction proteins, neurovascular and gliovascular microstructural rearrangements, and dysfunction associated with increased trafficking of inflammatory mediators and inflammatory cells from the periphery across the BBB leads to increase in the chronic neuroinflammatory reactions following brain injury. In this review, we advance the hypothesis that neuroinflammatory responses resulting from mast cell activation along with the accompanying risk factors such as age, gender, food habits, emotional status, stress, allergic tendency, chronic inflammatory diseases, and certain drugs can accelerate brain injury-associated neuroinflammation, neurodegeneration, and AD pathogenesis.

创伤性脑损伤 (TBI) 是美国的一个主要健康问题，每年影响约 170 万人。胶质细胞、T 细胞和肥大细胞在大脑的不同区域发挥特定的保护功能，以恢复包括 TBI 在内的中枢神经系统 (CNS) 损伤后的认知和运动功能。导致神经元死亡的慢性神经炎症反应以及脑损伤后伴随的压力会诱发或加速高危人群阿尔茨海默病 (AD) 的发病和进展。目前约有 570 万美国人患有 AD。脑损伤后，肥大细胞立即做出反应，释放预存和预激活的介质，并将免疫细胞招募到中枢神经系统。血脑屏障 (BBB)、紧密连接和粘附连接蛋白、神经血管和胶质血管微结构重排，以及与炎症介质和炎症细胞从外周跨 BBB 运输增加相关的功能障碍，导致脑损伤后慢性神经炎症反应增加。在这篇综述中，我们提出了这样的假设：肥大细胞激活引起的神经炎症反应以及伴随的危险因素，如年龄、性别、饮食习惯、情绪状态、压力、过敏倾向、慢性炎症性疾病和某些药物，可以加速脑损伤-相关的神经炎症、神经变性和 AD 发病机制。