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Alzheimer's disease (AD) is one of most devastating diseases affecting elderly people, Amyloid-�² (A�²) accumulation and
the downstream pathological events such as Tau phosphorylation play critical roles in ADpathogenesis. Edaravone is
marketed for acute ischemic stroke, has been proved for its capacity of inhibiting A�² aggregation and attenuating A�²-induced
oxidation in vitro. According to MTT assay, EDA has shown strong protection effect against cytotoxicity induced by CuSO4
and H2O2 on SY5Y695 cells. In the neurite outgrowth assay, the cortex neuron isolated from C57 pups were treated with 1uM
A�²42 in the presence of different concentration of EDA, data shows the neurite length of EDA 3uM group increased to 30%
to the control group and two folders high then the A�² only group. The PI staining apoptosis assay also indicated that cells
treated with EDA in differently concentration significantly reduced the death caused by CuSO4.In addition, P25/35 ratio is also
changed in EDA treatment group, in the 3uM EDA group, P35 expression is significant increase while P25 decease 2 folders.
Acetylcholinesterase (AChE) are enzymes that hydrolyze the neurotransmitter acetylcholine (ACh) to acetate and choline, the
AChE is often found to be highly active in AD pathology, according the AchE activity assay, the pilot result shows suppression
effect of EDA on AchE activity in vitro.
The ectodomain of p75 neurotrophin receptor (p75NTR-ECD) has been suggested to play important roles in regulating
beta-amyloid (A�²) deposition and in protecting neurons from the toxicity of soluble A�². Thus, we injected EDA and P75ECD
as a combination to treat AMY mice (AD model animal), we expect to see this combination can alleviates Alzheimer's diseasetype
pathologies and cognitive deficits.