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Abeta Predictor of Alzheimer Disease Symptoms
Chantelle F. Sephton, PhD;
Gang Yu, PhD
Arch Neurol. 2008;65(7):875-876.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings. |
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Alzheimer disease (AD) is a neurodegenerative disease characterized by a decline in cognitive function. The two major pathological features of this disease include extracellular β-amyloid (Aβ) plaques and intraneural neurofibrillary tangles. These pathological features seem to appear years before cognitive symptoms.1 Several hypotheses relate the pathological deteriorations in the brain of patients with AD to the mechanisms of neural degeneration. Among them, the amyloid hypothesis has emerged as a critical determinant of this pathology.2 According to this hypothesis, the neural degeneration that occurs in AD-affected brains is the consequence of Aβ hyperproduction and accumulation, resulting in Aβ deposits and leading to neuronal death. Since its proposal more than 15 years ago, numerous reports have strengthened the hypothesis that Aβ is the primary initiator of AD, but there are also many reports demonstrating that AD does not conform exactly to the amyloid hypothesis. For . . . [Full Text of this Article]AUTHOR INFORMATION
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