Abstract
Alzheimers disease (AD) is characterized pathologically by the overproduction or excessive accumulation of amyloid beta protein leading to the deposition of diffuse and neuriric plaques. Hyperphosphorylation of tau protein promotes the accumulation of intracellular neurofibrillary tangles. These events comprise a pathological cascade in the AD brain that includes oxidation, inflammation, excitotoxicity, and apoptosis with activation of myriad associated intracellular pathways. Some of these neuropathological changes are detectable by biomarkers such as neuroimaging or serum or cerebrospinal fluid (CSF) measures. Magnetic resonance imaging (MRI) reveals cerebral atrophy, fluorodeoxyglucose positron emission tomography (FDG-PET) shows regional brain hypometabolism, amyloid imaging demonstrates fibrillar amyloid in plaques, and CSF measures reveal decreased levels of the amyloid protein and increased levels of total tau protein and hyperphosphorylated tau. These biomarkers provide the basis for identifying and characterizing asymptomatic pre-clinical AD pathology, minimally symptomatic prodromal AD, and AD type dementia. Biomarkers have an increasingly important role in AD care and research at all stages of disease, and promise to assist in the development of new AD therapies.
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