Department of Pharmaceutical Sciences, College of Pharmacy, University of South Florida, Tampa, FL 33620, USA.
NutriFusion®, LLC, Naples, FL 34109, USA.
Nutrients. 2020 Dec 30;13(1):117. doi: 10.3390/nu13010117.
Alzheimer's disease (AD) is the result of the deposition of amyloid β (Aβ) peptide into amyloid fibrils and tau into neurofibrillary tangles. At the present time, there are no possible treatments for the disease. We have recently shown that diets enriched in phytonutrients show protection or limit the extent of damage in a number of neurological disorders. GrandFusion (GF) diets have attenuated the outcomes in animal models of traumatic brain injury, cerebral ischemia, and chronic traumatic encephalopathy. In this study, we investigated the effect of GF diets in a mouse model of AD prior to the development of amyloid plaques to show how this treatment paradigm would alter the accumulation of Aβ peptide and related pathologic changes (i.e., inflammation, cathepsin B, and memory impairment). Administration of GF diets (2-4%) over a period of four months in APP/ΔPS1 double-transgenic mice resulted in attenuation in Aβ peptide levels, reduction of amyloid load, and inflammation, increased cathepsin B expression, and improved spatial orientation. Additionally, treatment with GF diets increased nerve growth factor (NGF) levels in the brain and tempered the memory impairment in the animal model. These data suggest that GF diets may alter the development and progression of the mechanisms associated with the disease process to effectively modify AD pathogenesis.
阿尔茨海默病（AD）是由于β淀粉样肽（Aβ）在淀粉样纤维中的沉积和tau 在神经原纤维缠结中的沉积所致。目前，尚无针对该疾病的可能治疗方法。我们最近发现，富含植物营养素的饮食在许多神经疾病中具有保护作用或限制损伤的程度。GrandFusion（GF）饮食减轻了创伤性脑损伤、脑缺血和慢性创伤性脑病动物模型的结果。在这项研究中，我们在淀粉样斑块形成之前，在 AD 小鼠模型中研究了 GF 饮食的作用，以显示这种治疗模式如何改变 Aβ肽的积累和相关的病理变化（即炎症、组织蛋白酶 B 和记忆障碍）。在 APP/ΔPS1 双转基因小鼠中，GF 饮食（2-4%）的连续 4 个月给药可降低 Aβ肽水平、减少淀粉样蛋白负荷和炎症，增加组织蛋白酶 B 表达，并改善空间定向能力。此外，GF 饮食治疗可增加大脑中的神经生长因子（NGF）水平，并减轻动物模型的记忆障碍。这些数据表明，GF 饮食可能会改变与疾病过程相关的机制的发展和进展，从而有效地改变 AD 的发病机制。
