Oxidative stress, the imbalance of the antioxidant system, results in an accumulation of neurotoxic proteins in Alzheimer's disease (AD). The antioxidant system is composed of exogenous and endogenous antioxidants to maintain homeostasis. Superoxide dismutase (SOD) is an endogenous enzymatic antioxidant that converts superoxide ions to hydrogen peroxide in cells. SOD supplementation in mice prevented cognitive decline in stress-induced cells by reducing lipid peroxidation and maintaining neurogenesis in the hippocampus. Furthermore, SOD decreased expression of BACE1 while reducing plaque burden in the brain. Additionally, Astaxanthin (AST), a potent exogenous carotenoid, scavenges superoxide anion radicals. Mice treated with AST showed slower memory decline and decreased depositions of amyloid-beta (Aβ) and tau protein. Currently, the neuroprotective potential of these supplements has only been examined separately in studies. However, a single antioxidant cannot sufficiently resist oxidative damage to the brain, therefore, a combinatory approach is proposed as a relevant therapy for ameliorating pathological changes in AD.

氧化应激，即抗氧化系统的失衡，导致阿尔茨海默病 (AD) 中神经毒性蛋白的积累。抗氧化系统由外源性和内源性抗氧化剂组成，以维持体内平衡。超氧化物歧化酶 (SOD) 是一种内源性酶抗氧化剂，可在细胞中将超氧离子转化为过氧化氢。小鼠中的 SOD 补充剂通过减少脂质过氧化和维持海马中的神经发生来防止应激诱导细胞的认知能力下降。此外，SOD 降低了 BACE1 的表达，同时减少了大脑中的斑块负荷。此外，虾青素 (AST) 是一种有效的外源性类胡萝卜素，可清除超氧阴离子自由基。用 AST 治疗的小鼠表现出较慢的记忆衰退和减少的淀粉样蛋白沉积（A β) 和 tau 蛋白。目前，仅在研究中单独检查了这些补充剂的神经保护潜力。然而，单一的抗氧化剂不能充分抵抗对大脑的氧化损伤，因此，提出了一种组合方法作为改善 AD 病理变化的相关疗法。