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Editorials |
Departments of1 Pathology (Neuropathology) and2 Neurology, University of Virginia Health System Charlottesville, VA
aAddress correspondence to this author at: Department of Pathology (Neuropathology), University of Virginia Health System, Charlottesville, VA, 22908. Fax 434-924-9177; e-mail jwm2m@virginia.edu.
| The first 20% of the full text of this article appears below. |
Alzheimer disease (AD), the most common form of dementia, is a neurodegenerative disorder characterized by neuronal and synaptic loss. Despite its high prevalence and great cost to society, there is no definitive premortem test for AD (1)(2). The diagnosis of probable or possible AD is based on a history of insidious onset and progressive impairment of memory as well as loss of other cognitive functions (3). The most important clinical task is the exclusion of reversible causes of dementia, most commonly vascular dementia. It is of little comfort to treating physicians and family members that postmortem examination of the brain by the pathologist is the only reliable diagnostic test for AD. Typically, microscopic examination of stained sections of brain taken from cortical and limbic brain regions reveals the hallmark changes of AD, namely, accumulation of intracellular neurofibrillary tangles and extracellular amyloid plaques. Neurofibrillary tangles are composed mainly of abnormally hyperphosphorylated tau protein (P-TAU). The extracellular amyloid plaques are composed of the 40- and 42-amino acid-long ß-amyloid peptides [Aß(140) and Aß(142)]. Several neuropathologic subtypes of AD have been described, depending principally on the cortical regions most affected by neuronal loss, and the
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