| Literature DB >> 31565701 |
Willam T Wang1, Breeya A Tailor2, David S Cohen2, Xudong Huang2.
Abstract
Alzheimer's disease (AD) characterized by insoluble amyloid-β (Aβ) deposits, neurofibrillary tangles (NFTs), and neuronal demise. The influence of environmental and genetic factors on AD progression remains elusive, however evidence suggests biometal dyshomeostasis elicits neuronal death, neuroinflammation, and accumulated oxidative damages in AD brain. As such, three pathways have been identified that result from abnormal biometal accumulation and increased levels of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in AD brain parenchyma: (1) the damage caused by direct oxidation of cellular components such as DNA and proteins; (2) the oligomerization of Aβ and NFTs, and (3) the promotion of apoptosis through NF-κB signaling pathway. Finally, given recent developments in nanotechnology, we have briefly reviewed potential nanotheranostic agents as potential AD theranostics.Entities:
Keywords: Alzheimer’s Disease; Aβ Amyloid; Biometals; Blood-Brain Barrier; Metal Chelators; Nanotheranostics; Redox Stress; Tau Protein
Year: 2019 PMID: 31565701 PMCID: PMC6764777
Source DB: PubMed Journal: EC Pharmacol Toxicol