Fig. (4) A proposed model of AD neurodegeneration through the stress-activated p38K and apoptosis. Oxidative stress induces the activation of p38K and its upstream effector, MKK6. Activated (phosphorylated) p38K will then phosphorylate Bax in the cytoplasm, causing its translocation to mitochondria to initiate the mitochondria-dependent apoptosis process, and then ultimately neurodegeneration. In addition, activated p-P38K can also phosphorylate Tau protein, causing aggregations called neurofibrillary tangles, which also contribute to neurodegeneration. This model is similar to those previously reported [43-45].