Tau protein and amyloid s (Abeta), two major components of neuropathology in Alzheimer disease (AD), have been applied for establishment of more useful biomarkers and therapeutic approaches. Total tau protein in CSF is a biomarker for AD, however increased levels of total tau in CSF were also observed in other neurological disease with dementia. Phosphorylation is an important feature of tau protein and phosphorylated tau in CSF is useful to distinguish AD from other disease. Abeta has toxic effects on neuronal cells, and its mechanisms are complicated. One of mechanism of Abeta-cytotoxicity is a down-regulation of XIAP, and this effect is observed in the low concentration of Abeta. XIAP might be a therapeutic target employing compounds that increase expression of XIAP in neuronal cells.