Fig. 1

The myeloproliferative blood cancers—essential thrombocytosis (ET), polycythemia vera (PV), and myelofibrosis (MF)—(MPNs) evolve in a biological continuum, spanning 5-10-20 years from the early cancer stages (ET/PV) towards the advanced MF stage. Chronic inflammation is the driving force for this development giving rise to increasing oxidative stress and increasing genomic instability. Inflammatory cytokines drive clonal evolution, and the clone itself generates oxidative stress and inflammatory products which in a self-perpetuating vicious circle elicits more fuel to the fire. In the initial stages of MPNs (ET, PV, and hyperproliferative MF), blood cell counts are elevated (in PV always red blood cells but very often leukocytes and platelets as well, in ET always elevated platelet counts and in some patients elevated leukocyte counts as well and in MF elevated leukocyte and platelet counts). Neuroinflammation is associated with several chronic inflammatory diseases. It is argued that chronic systemic inflammation in MPNs may also elicit neuroinflammation in MPNs and contribute to the CNS-symptom burden in patients with MPNs. It is hypothesized that MPNs are “A Human Neuroinflammation Model” for Alzheimer’s disease development