Journal
JOURNAL OF NEUROCHEMISTRY
Volume 91, Issue 3, Pages 513-520Publisher
BLACKWELL PUBLISHING LTD
DOI: 10.1111/j.1471-4159.2004.02737.x
Keywords
amyloid; intraneuronal beta-amyloid; neurodegeneration; oligomers; post mortem; transgenic mice
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Accumulating evidence points to an important role of intraneuronal Abeta as a trigger of the pathological cascade of events leading to neurodegeneration and eventually to Alzheimer's disease (AD) with its typical clinical symptoms, like memory impairment and change in personality. In the present article, we review recent findings on intracellular monomeric and oligomeric beta-amyloid (Abeta) generation and its pathological function in cell culture, transgenic AD mouse models and post mortem brain tissue of AD and Down syndrome patients, as well as its interaction with oxidative stress and its relevance in apoptotic cell death. Based on these results, a modified Abeta hypothesis is formulated, that integrates biochemical, neuropathological and genetic observations with AD-typical neuron loss and plaque formation.
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