Cover Story：Alzheimer's disease (AD) is currently an incurable neurodegenerative disease, which is the most common cause of dementia worldwide. AD is also a progressive disorder, pathologically characterized by extracellular amyloid beta plaques and intracellular neurofibrillary tangles (NFTs). NFTs consist of paired helical filaments of microtubule-associated tau protein that is hyperphosphorylated and the density of tau tangles correlates well with regional and global aspects of AD-associated cognitive dysfunction. Furthermore, the established toxic role of tau in certain genetic forms of frontotemporal dementia strongly suggests that tau aggregation may result in a toxic gain-of-function leading to the AD-associated neurodegeneration. Thus, there is a growing interest in discovering novel compounds that will help in reducing the deleterious accumulation of tau protein tangles in the AD brain. Stem cells treatment open a gate to this which many drugs show hard to control the disease progression or enhance the patients' consideration function. hUC-MSCs (mesenchymal stem cells isolated from human Wharton's jelly of unbilical cord), emphasized by its powerful paracrine, great function of multi-directional differentiation and east to isolate, have been confirmed effective to many nervous system disease including AD. But the treatment mechanism was still unknown. Along with the studies of secreted factors by hUC-MSCs, the paracrine function of the adult stem cells attracted us to answer this treatment mechanism from those star factors. Here, we set up the AD model in vitro by okadaic acid (OA), and demonstrate that IL-6 maybe the key protein to effect the recovery function of hUC-MSCs to protect the injured cells.