纳米材料干预神经退行性疾病中的蛋白质错误折叠与神经炎症

Neurodegenerative disorders such as Alzheimer's disease are characterized by pathological protein misfolding, persistent neuroinflammation, and progressive synaptic deterioration. Nanoscale therapeutic platforms offer a versatile strategy for simultaneously suppressing pathogenic protein aggregation and modulating glial hyperactivation, thereby addressing the multifactorial nature of neurodegenerative pathology. Engineered AuNPs, carbon-based nanodots, and related constructs with negatively charged surfaces exhibit high affinity for amyloidogenic peptides, thereby limiting amyloid-β or tau fibrillization, while photothermal strategies using graphene or gold nanorods induce localized thermal disruption of preformed aggregates, enhancing their disassembly. In parallel, functionalized nanocarriers facilitate brain-targeted delivery of anti-inflammatory agents by leveraging receptor-mediated transcytosis or biomimetic cell membrane-camouflaging strategies, attenuating proinflammatory cytokines and promoting autophagic clearance. <i>In vitro</i> and <i>in vivo</i> models demonstrate integrated therapeutic benefits, including attenuation of plaque deposition, preservation of neuronal integrity, and recovery of cognitive performance. Despite remaining challenges in large-scale synthesis and long-term safety, evolving nanotechnologies offer a flexible and integrated platform capable of disrupting the pathogenic cycle linking protein misfolding, neuroinflammation, and disease progression.