CSF biomarkers of AD: monitoring therapeutic targets

grounds, implying the presence of senile plaques and neurofibrillary tangles in the hippocampus and cerebral cortex. Brain autopsy studies indicate that these lesions are present in about 90% of patients clinically diagnosed by experienced physicians. The utility of biomarkers for enhancing diagnositic sensitivity for AD may consequently be relatively limited since clinical methods are generally reliable. Although biomarkers are also unlikely to alter treatment decisions about the currently available therapies (i.e., cholinesterase inhibitors and NMDA antagonists), biomarkers may serve as indices of disease activities (e.g., inflammation, oxidative damage, "nitrosative" damage, astrocytic activation, and neuronal damage or death) which are targets of future therapeutic intervention. Amyloid plaque and neurofibrillary tangle formation are other mechanisms in this category, and measurement of these mechanisms has been attempted with assays for beta amyloid 1-42, tau, and phospho-tau, which have been described in numerous publications and reviews. The present manuscript will focus on AD biomarkers other than beta amyloid and tau.