Blood will out: vascular contributions to Alzheimer’s disease
Sidney Strickland
Patricia and John Rosenwald Laboratory of Neurobiology and Genetics, The Rockefeller University, New York, New York, USA.
Address correspondence to: Sidney Strickland, Laboratory of Neurobiology and Genetics, 1230 York Avenue, New York, New York 10021, USA. Phone: 212.327.8705; Email: strickland@rockefeller.edu.
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First published February 1, 2018 - More info
J Clin Invest. 2018;128(2):556–563. https://doi.org/10.1172/JCI97509.
Copyright © 2018, American Society for Clinical Investigation
The fundamental pathology in Alzheimer’s disease (AD) is neuronal dysfunction leading to cognitive impairment. The amyloid-β peptide (Aβ), derived from amyloid precursor protein, is one driver of AD, but how it leads to neuronal dysfunction is not established. In this Review, I discuss the complexity of AD and possible cause-and-effect relationships between Aβ and the vascular and hemostatic systems. AD can be considered a multifactorial syndrome with various contributing pathological mechanisms. Therefore, as is routinely done with cancer, it will be important to classify patients with respect to their disease signature so that specific pathologies, including vascular pathways, can be therapeutically targeted.
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Copyright © 2018 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)