A 75-year-old man had a 1-year history of progressive memory problems.

Our patient had difficulties with short-term memory. His wife noted that her husband had troubles with simple calculations and remembering recent conversations. On one occasion, while staying at an unfamiliar environment, he became confused, unclothed, and attempted to enter the hotel rooms of other guests. Past medical history was notable for pulmonary fibrosis and hyperlipidemia. He had no history of previous stroke, head trauma, or central nervous system (CNS) infection. He did not drink alcohol excessively and was on no medications that could impair cognition. There was no family history of dementia.

On examination, he was oriented to person, place, and time except that he had difficulty naming the month. Immediate recall and attention were unremarkable. He was able to name two of three objects on testing short-term recall. He was not aphasic, was able to follow multistep commands, and had no construction apraxia. He was diagnosed as having early Alzheimer disease and treated with galantamine.

Dementia is defined as a decline in memory and at least one other cognitive domain impairing social or occupational functioning. Dementia results from many causes including degenerative, vascular, infectious, psychiatric, toxic, metabolic, traumatic, and brain structural etiologies. Most nondegenerative causes can be excluded with appropriate history and a thorough general and neurologic examination, neuroimaging, and laboratory
evaluation. Neuropsychologic testing further defines the specific cognitive abnormalities. The most common cause of dementia is Alzheimer disease. Hippocampal, mesial temporal lobe, and parietal lobe atrophy may be seen on computed tomography (CT) or magnetic resonance imaging (MRI). Positron emission tomography (PET) may demonstrate bilateral temporoparietal hypometabolism. More recently, the use of biomarkers in the diagnosis of Alzheimer disease has received considerable attention in the literature, including abnormal Aβ metabolism as demonstrated by low amyloid β-42 (with high phosphorylated tau) on cerebrospinal fluid (CSF) and increased uptake on the Pittsburgh compound B (PIB PET) of fibrillar Aβ of senile plaques in neocortical regions.