The current diagnosis of Alzheimer disease is made by clinical, neuropsychological, and neuroimaging assessments. Routine structural neuroimaging evaluation has long been based on nonspecific features such as atrophy, which is a late feature in the progression of the disease. More recently, a variety of imaging modalities, including structural and functional magnetic resonance imaging (MRI) and positron emission tomography (PET) studies of cerebral metabolism, have shown characteristic changes in the brains of patients with Alzheimer disease in prodromal and even presymptomatic states. [1, 2, 3]
Alzheimer disease was first described in 1907 by Alois Alzheimer. From its original status as a rare disease, Alzheimer disease has become one of the most common diseases in the aging population, ranking as the fourth most common cause of death. Alzheimer disease is a progressive neurodegenerative disorder characterized by the gradual onset of dementia. The pathologic hallmarks of the disease are beta-amyloid (Aβ) plaques, neurofibrillary tangles (NFTs), and reactive gliosis. [4, 5, 6] (See the images below.)
Coronal, T1-weighted magnetic resonance imaging (MRI) scan in a patient with moderate Alzheimer disease. Brain image reveals hippocampal atrophy, especially on the right side.
Axial, T2-weighted magnetic resonance imaging (MRI) scan of the brain reveals atrophic changes in the temporal lobes.
Structural imaging, preferably with MRI when possible and computed tomography (CT) when not, should be obtained as a first-tier approach. MRI can be considered the preferred neuroimaging examination for Alzheimer disease because it allows for accurate measurement of the 3-dimensional (3D) volume of brain structures, especially the size of the hippocampus and related regions. Second-tier imaging with molecular methods, preferably with fluorodeoxyglucose PET (or single-photon emission CT if PET is unavailable) can provide more diagnostic specificity. 
Neuroimaging is widely believed to be generally useful for excluding reversible causes of dementia syndrome, such as normal-pressure hydrocephalus, brain tumors, and subdural hematoma, and for excluding other likely causes of dementia, such as cerebrovascular disease. 
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