Park Hyoungshin, Ni Mya, Le Yvonne
Department of Biology, School of Arts and Sciences, Massachusetts College of Pharmacy and Health Sciences, Boston, MA, United States.
Front Neurol. 2025 Jul 23;16:1622571. doi: 10.3389/fneur.2025.1622571. eCollection 2025.
The brain contains approximately 100 billion neurons and over 200 billion glial cells, which are integral to the neuronal networks that support normal brain function in the central nervous system. The complexity of the brain makes the diagnosis and treatment of neurodegenerative disease particularly challenging. Neuroinflammation and neuronal cell death contribute to the development of neurodegenerative diseases such as dementia. Dementia refers to a decline in memory and thinking ability, affecting approximately 55 million people worldwide. Owing to the association of multiple factors, including amyloid- plaque, tau-fibrillary tangles, neuroinflammation, nutritional defects, and genetic mutations, the exact cause of the most common type of dementia, Alzheimer's disease, remains elusive. These multiple factors may cause damage to neurons and glial cells, leading to neurodegeneration. Very few therapeutics are available for neurodegenerative diseases due to the limited understanding of their pathogenesis, resulting in the lack of biomarkers and drug targets. Recent attention has shifted toward addressing modifiable risk factors such as unhealthy diets and lifestyles to delay the onset of Alzheimer's disease. Unhealthy diets that consist of saturated fatty acids and refined sugars, with other multiple risk factors, increase neuroinflammation and oxidative stress, furthering cognitive decline and progression of neurodegeneration. Mitigating these risk factors with antioxidants, anti-inflammatory-based nutrition, and multidomain lifestyle intervention, which may include physical exercise, cognitive stimulation, and social engagement, may delay the development of neurodegenerative diseases and cognitive decline. In this review, we focus on the role of neuroinflammation in contributing to neurodegeneration and dietary influence in Alzheimer's disease.
大脑包含约1000亿个神经元和超过2000亿个神经胶质细胞,它们是支持中枢神经系统正常脑功能的神经网络所不可或缺的。大脑的复杂性使得神经退行性疾病的诊断和治疗极具挑战性。神经炎症和神经元细胞死亡会导致诸如痴呆症等神经退行性疾病的发展。痴呆症是指记忆和思维能力下降,全球约有5500万人受其影响。由于多种因素的关联,包括淀粉样斑块、tau蛋白纤维缠结、神经炎症、营养缺陷和基因突变,最常见的痴呆类型——阿尔茨海默病的确切病因仍不清楚。这些多种因素可能会对神经元和神经胶质细胞造成损害,导致神经退行性变。由于对神经退行性疾病发病机制的了解有限,针对这些疾病的治疗方法非常少,这导致缺乏生物标志物和药物靶点。最近,人们的注意力已转向解决可改变的风险因素,如不健康的饮食和生活方式,以延缓阿尔茨海默病的发病。由饱和脂肪酸和精制糖组成的不健康饮食,与其他多种风险因素一起,会增加神经炎症和氧化应激,进一步加剧认知能力下降和神经退行性变的进展。通过抗氧化剂、基于抗炎的营养以及多领域生活方式干预(可能包括体育锻炼、认知刺激和社交参与)来减轻这些风险因素,可能会延缓神经退行性疾病的发展和认知能力下降。在这篇综述中,我们重点关注神经炎症在导致神经退行性变中的作用以及饮食对阿尔茨海默病的影响。