作者: Jan Aaseth , Jan Alexander , Geir Bjørklund , Knut Hestad , Petr Dusek
DOI: 10.1007/S10534-016-9959-8
关键词:
摘要: Alzheimer’s disease (AD) is a neurodegenerative disorder presenting one of the biggest healthcare challenges in developed countries. No effective treatment exists. In recent years main focus AD research has been on amyloid hypothesis, which postulates that extracellular precipitates beta (Aβ) derived from precursor protein (APP) are responsible for cognitive impairment seen AD. Treatment strategies have to reduce Aβ production through inhibition enzymes its formation, or promote resolution existing cerebral plaques. However, these approaches failed demonstrate significant improvements. Intracellular rather than events may be fundamental pathogenesis. Selenate potent inhibitor tau hyperphosphorylation, critical step formation neurofibrillary tangles. Some selenium (Se) compounds e.g. selenoprotein P also appear protect APP against excessive copper and iron deposition. Selenoproteins show anti-inflammatory properties, microtubules neuronal cytoskeleton. Optimal function selenoenzymes requires higher Se intake what common Europe traditionally recommended. Supplementary with N-acetylcysteine increases levels antioxidative cofactor glutathione can mediate adjuvant protection. The present review discusses role suggests prevention by optimizing intake, accordance metal dysregulation hypothesis. This includes particular secondary supplementation elderly mild impairment.