Naik Rayees Ahmad, Mir Mehak Naseer, Malik Ishfaq Ahmad, Bhardwaj Rima, Alshabrmi Fahad M, Mahmoud Mahmoud Abdulrahman, Alhomrani Majid, Alamri Abdulhakeem S, Alsanie Walaa F, Hjazi Ahmed, Ghatak Tanmoy, Poeggeler Burkhard, Singh Mahendra P, Ts Gopenath, Singh Sandeep Kumar
Department of Zoology, Dr. Harisingh Gour Vishwavidyalaya Sagar, 470003 Sagar, Madhya Pradesh, India.
NIMS Institute of Allied Medical Science, National Institute of Medical Sciences (NIMS), 303121 Jaipur, Rajasthan, India.
Front Biosci (Landmark Ed). 2025 Feb 18;30(2):25551. doi: 10.31083/FBL25551.
Alzheimer's disease (AD) is the most prevalent cause of dementia and a significant contributor to health issues and mortality among older individuals. This condition involves a progressive deterioration in cognitive function and the onset of dementia. Recent advancements suggest that the development of AD is more intricate than its underlying brain abnormalities alone. In addition, Alzheimer's disease, metabolic syndrome, and oxidative stress are all intricately linked to one another. Increased concentrations of circulating lipids and disturbances in glucose homeostasis contribute to the intensification of lipid oxidation, leading to a gradual depletion of the body's antioxidant defenses. This heightened oxidative metabolism adversely impacts cell integrity, resulting in neuronal damage. Pathways commonly acknowledged as contributors to AD pathogenesis include alterations in synaptic plasticity, disorganization of neurons, and cell death. Abnormal metabolism of some membrane proteins is thought to cause the creation of amyloid (Aβ) oligomers, which are extremely hazardous to neurotransmission pathways, especially those involving acetylcholine. The interaction between Aβ oligomers and these neurotransmitter systems is thought to induce cellular dysfunction, an imbalance in neurotransmitter signaling, and, ultimately, the manifestation of neurological symptoms. Antioxidants have a significant impact on human health since they may improve the aging process by combating free radicals. Neurodegenerative diseases are currently incurable; however, they may be effectively managed. An appealing alternative is the utilization of natural antioxidants, such as polyphenols, through diet or dietary supplements, which offer numerous advantages. Within this framework, we have extensively examined the importance of oxidative stress in the advancement of Alzheimer's disease, as well as the potential influence of antioxidants in mitigating its effects.
阿尔茨海默病（AD）是痴呆症最常见的病因，也是导致老年人健康问题和死亡的重要因素。这种疾病涉及认知功能的逐渐衰退和痴呆症的发作。最近的研究进展表明，AD的发展比单纯的潜在脑异常更为复杂。此外，阿尔茨海默病、代谢综合征和氧化应激之间都存在着复杂的联系。循环脂质浓度的增加和葡萄糖稳态的紊乱会导致脂质氧化加剧，从而导致机体抗氧化防御能力逐渐耗尽。这种增强的氧化代谢会对细胞完整性产生不利影响，导致神经元损伤。通常被认为是AD发病机制促成因素的途径包括突触可塑性的改变、神经元的紊乱和细胞死亡。一些膜蛋白的异常代谢被认为会导致淀粉样蛋白（Aβ）寡聚体的产生，这些寡聚体对神经传递途径，尤其是涉及乙酰胆碱的途径极其有害。Aβ寡聚体与这些神经递质系统之间的相互作用被认为会诱导细胞功能障碍、神经递质信号失衡，并最终导致神经症状的出现。抗氧化剂对人类健康有重大影响，因为它们可以通过对抗自由基来改善衰老过程。神经退行性疾病目前无法治愈；然而，可以有效地进行管理。一个有吸引力的替代方法是通过饮食或膳食补充剂使用天然抗氧化剂，如多酚，它们具有许多优点。在此框架内，我们广泛研究了氧化应激在阿尔茨海默病进展中的重要性，以及抗氧化剂在减轻其影响方面的潜在作用。
