Cortes-Canteli M, Paul J, Norris EH, Bronstein R, Ahn HJ, Zamolodchikov D, Bhuvanendran S, Fenz KM, Strickland S. Fibrinogen and beta-amyloid association alters thrombosis and fibrinolysis: a possible contributing factor to Alzheimer's disease. Neuron. 2010 Jun 10;66(5):695-709. PubMed.
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NYU Medical Center
Regarding the true primary cause of Alzheimer's, the full pathway must be elucidated from start to finish. But it's important to consider that not every etiologic mechanism is therapeutically tractable. Sometimes it is better to approach a disease pathway using points downstream. Dysregulation of fibrinogen, amyloid-β, or some other molecule, may prove to be the initial driving force in this disease, but impaired blood flow could still be the best therapeutic target to improve cognition.
We already know that impaired blood flow can affect cognition. Alzheimer's may present a very subtle form of this, but we must keep our attention on the basic goal of therapy—to improve brain function. In medical school, I saw many patients diagnosed with Alzheimer's, and none of them first came to the physician complaining of plaques and tangles. They complained of problems with memory and cognition. We must always consider this when making strides in translational, "bench-to-bedside" research.
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