Neurodegeneration, such as Alzheimer's disease (AD) can progress over decades before dementia becomes apparent. Imaging, cerebrospinal fluid (CSF) and blood-based biomarkers have the potential to improve the accuracy by which specific causes of dementiacan be diagnosed in vivo, provide insights into the underlying pathophysiology, and may be used as inclusion criteria and outcome measures for clinical trials. 
　　At present there are several? biochemical measurements or scanning procedures are used as biomarkers, usually in panels, by neurologists and others. The biochemical measurements are principally of amyloid proteins and their A-beta precursors, or of tau proteins. Brain atrophy can be assessed by means of structural magnetic resonance imaging (sMRI), and decreased blood flow and metabolism can be estimated by functional magnetic resonance imaging (fMRI). [18F]fluorodeoxyglucose-positron emission tomography (FDG-PET) is used to measure the brain's energy utilization and to infer synaptic number.
　　The temporal ordering model of AD biomarkers varying across individuals because of genetic/environmental factors that increase/decrease resilience to AD pathologies. These features are reflected in the AD cerebrospinal fluid (CSF) by increased concentrations of total tau (t-tau) and phosphorylated tau (p-tau), together with decreased concentrations of β-amyloid (Aβ42), respectively. In combination, Aβ42, p-tau and t-tau are 85-95% sensitive and specific for AD in both prodromal and dementiastages of the disease and they are now included in the diagnostic research criteria for AD. However, to fully implement these biomarkers into clinical practice, harmonization of data is needed.
　　The clinical usefulness of established AD biomarkers, Aβ and tau, could be further improved by developing an algorithm. Such biomarker algorithm could aid in early detection and intervention as well as identify novel treatment targets to delay disease onset, slow progression, and/or prevent AD.