The amyloid hypothesis of the development of Alzheimer's disease (AD) continues to dominate, though the concept has changed significantly during its 25-year history. The accumulation of β-amyloid has been found to be linked not only with increase in its production (as found after elucidation of the genetic mechanisms of some familial cases of AD), but also with impairments to its clearance from brain tissues, which is mediated by the microcirculatory system. The most significant pathogenetic role in brain substance is played not by the senile plaques themselves, described by Alois Alzheimer almost 110 years ago and consisting of insoluble conjugates, but by soluble β-amyloid oligomers. The relationship between the vascular and degenerative processes in AD is supported by the common risk factors and by clinical, neuroimaging, pathomorphological, and experimental data. One component linking degenerative and vascular processes in AD is insulin resistance. Challenges of new multimodal therapeutic strategies for AD are discussed in relation to the current status of the amyloid hypothesis.
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