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With the advent of potential disease modifying agents, early identification and diagnosis of individuals with Alzheimers disease (AD) is critical.Unfortunately, patients with Mild Cognitive Impairment (MCI) and mild dementia due to AD typically do not present to their family doctor for an average of 3.5 years after symptoms are obvious to others.Patients do not seek evaluation due to impaired insight and families are hesitant to bring up the issue.Physicians may not notice subtle cognitive deficits if not looking for them.Early identification of Alzheimers disease may led to earlier treatments, enhanced patient supervision, and improved treatment compliance rates for other chronic medical conditions.The earliest biomarker signal for AD is amyloid-beta accumulation in the brain (CSF/PET), followed by evidence of synaptic dysfunction (PET), tau-mediated neuronal injury (CSF), brain atrophy (MRI), cognitive impairment, and finally functional impairment.The most commonly used CSF biomarkers for AD include reduced beta amyloid 42 peptide and elevated tau protein with the combination providing 86% specificity and 85% sensitivity for AD compared to controls.Functional imaging using flurodeoxy glucose (FDG) PET shows bilateral temporal and parietal hypometabolism in AD and predicts the risk of progression to AD dementia in MCI subjects in 94% after 3 years.MRI volumetric measurement of hippocampus and entorhinal cortex atrophy is 95% sensitive but only 40% specific for AD dementia.Amyloid PET imaging (eg.Florbetapir) to identify brain amyloid shows significantly more uptake in AD than MCI subjects or controls.Screening with mental status testing for early identification is suggested.New screening tools like the Self-Administered Gerocognitive Examination (SAGE) in validity studies has shown 95% specificity and 79% sensitivity to detect cognitive impairment from normal subjects.