Abstract
Alzheimer’s disease (AD) is pathologically characterized by excessive accumulation of amyloid-beta (Aβ) within extracellular spaces of the brain. Aggregation of Aβ has been shown to trigger oxidative stress, inflammation, and neurotoxicity resulting in cognitive dysfunction. In this study, we use models of cerebral Aβ amyloidosis to investigate anti-amyloidogenic effects of scutellarin in vitro and in vivo. Our results show that scutellarin, through binding to Aβ42, efficiently inhibits oligomerization as well as fibril formation and reduces Aβ oligomer-induced neuronal toxicity in cell line SH-SY5Y. After nine months of treatment in APP/PS1 double-transgenic mice, scutellarin significantly improves behavior, reduces soluble and insoluble Aβ levels in the brain and plasma, decreases Aβ plaque associated gliosis and levels of proinflammatory cytokines TNF-α and IL-6, attenuates neuroinflammation, displays anti-amyloidogenic effects, and highlights the beneficial effects of intervention on development or progression of AD-like neuropathology.
Highlights
Alzheimer diseases (AD) is the most common kind of neurodegeneration disease in the elderly, characterized by deterioration of cognitive functions, extracellular Aβ deposits and intracellular neurofibrillary tangles, other pathology features include the cholinergic neurons and synaptic degeneration/loss, cerebral amyloid angiopathy (CAA), neuroinflammation, and oxidative damage [1,2].Alzheimer’s disease (AD) is so chronic and complex disease
Bioscience, which was dissolved in HFIP at a concentration of 1 mg/mL and was separated into aliquots in sterile Eppendorf Tube (100 μg/tube), followed by incubation at room temperature for 24 h in the fume hood to form clear peptide film, the resulting peptide films were dried under vacuum overnight and stored at −20 ◦ C before assaying [7]
Some research conclusions indicate that scutellarin is an effective compound for the prevention of AD-like neuropathology
Summary
AD is so chronic and complex disease. There is no current disease-modifying therapy available for the treatment of this disorder. In spite of extensive academic, pharmaceutical, and medicinal research, numerous drug candidates targeting Aβ or β-secretase have failed in clinical trials. This means drugs with single targets have less therapeutic effects or cause side effects when used to prevent or treat AD. The new strategy towards development of safe agents with multiple targets, natural polyphenols are likely to comply with these requirements due to the advantages of multi-target effects and fewer side effects
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