Molecular nutrition & food research · 2018
Se-Methylselenocysteine Ameliorates Neuropathology and Cognitive Deficits by Attenuating Oxidative Stress and Metal Dyshomeostasis in Alzheimer Model Mice.
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Xie Yongli, Liu Qiong, Zheng Lin, Wang BingTao, Qu Xiaogang, Ni Jiazuan, Zhang Yan, Du Xiubo
Аннотация
SCOPE: Se-methylselenocysteine (SMC) is a major selenocompound in selenium (Se)-enriched plants. Se is vital for proper brain function, and Se-deficient is considered to be related with cognitive impairment and Alzheimer's disease (AD). The potential of SMC in intervening cognitive deficits and neuropathology of triple transgenic AD (3 × Tg-AD) mice is evaluated for the first time.
METHODS AND RESULTS: AD mice are treated with SMC (0.75 mg kg-1 BW per day) in their drinking water for 10 months. Results reveal that SMC 1) reduces oxidative stress and neuro-inflammation; 2) modulates the distribution and levels of several metal ions; 3) decreases amyloid-β peptide (Aβ) generation by inhibiting the expression of its precursor protein APP and β-secretase (BACE1); and 4) attenuates tau hyperphosphorylation and neurofibrillary tangles (NFT) formation via promoting protein phosphatase 2A (PP2A) activity, thereby preserving synaptic proteins and neuron activities and finally improving spatial learning and memory deficits in AD model mice. The authors suggest that the inhibitory effect of SMC on MEK/ERK activation may play a critical role in intervening AD progression.
CONCLUSIONS: These results reveal that SMC is powerful in ameliorating AD-related neuropathology and cognitive deficits via modulating oxidative stress, metal homeostasis, and extracellular signal-regulated kinase (ERK) activation.
METHODS AND RESULTS: AD mice are treated with SMC (0.75 mg kg-1 BW per day) in their drinking water for 10 months. Results reveal that SMC 1) reduces oxidative stress and neuro-inflammation; 2) modulates the distribution and levels of several metal ions; 3) decreases amyloid-β peptide (Aβ) generation by inhibiting the expression of its precursor protein APP and β-secretase (BACE1); and 4) attenuates tau hyperphosphorylation and neurofibrillary tangles (NFT) formation via promoting protein phosphatase 2A (PP2A) activity, thereby preserving synaptic proteins and neuron activities and finally improving spatial learning and memory deficits in AD model mice. The authors suggest that the inhibitory effect of SMC on MEK/ERK activation may play a critical role in intervening AD progression.
CONCLUSIONS: These results reveal that SMC is powerful in ameliorating AD-related neuropathology and cognitive deficits via modulating oxidative stress, metal homeostasis, and extracellular signal-regulated kinase (ERK) activation.