Fig. 3

The myeloproliferative blood cancers, MPNs, are associated with chronic inflammation and oxidative stress, which drive the malignant clone from the early cancer stages—ET and PV—towards the advanced burnt-out myelofibrosis stage with bone marrow failure. Smoking is a known risk factor for both MPN- and Alzheimer’s disease (AD) development. By triggering the NF-kB and JAK-STAT pathways, smoking elicits the production of several proinflammatory cytokines, including IL-6, IL-8, and TNF-alpha, which are released from leukocytes and platelets and also give rise to leukocyte-, platelet, and endothelial cell activation. A huge amount of amyloid beta is released from circulating activated platelets. Taking into account that the above pathways are activated in MPNs and AD as well, and the MPNs and AD share a similar inflammatory landscape, it is intriguing to consider, if leukocyte and platelet activation together with chronic inflammation and oxidative stress may constitute the common links, which are determinant for eliciting neuroinflammation, capillary stalling due to plugging of the microcirculation with activated blood cells and ultimately decreased cerebral blood flow and AD development