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Updated: Feb 6, 2026
Transduction-Transplantation Mouse Model of Myeloproliferative Neoplasm
Published on: December 22, 2016
Reorganization of the sensorimotor cortex in patients with Ph-negative myeloproliferative neoplasms according to
Polina I Kuznetsova1, Sofya N Morozova2, Anton A Raskurazhev1
1Laboratory of Neuropharmacological fMRI, 1st Neurological Department (Angioneurology), Russian Center of Neurology and Neurosciences, Moscow, Russia.
Introduction:
Myeloproliferative neoplasms (MPN) may contribute to cerebrovascular disease via cellular and endothelial pathology leading to impairment at the neurovascular unit (NVU) level. Studies targeting this patient cohort form a neuroscientific viewpoint are scarce.
Objective:
We aimed at elucidating possible neuroimaging correlates of NVU alterations in MPNs patients.
Materials And Methods:
We initially included 187 patients with MPNs in this study, retaining 39 patients as per eligibility criteria (25.6% males, median age - 43 years), who were matched with a control group of 11 healthy subjects (36.4% males, median age - 41 years). Structural and task-based (motor paradigm) functional MRI were performed in both groups, along with the evaluation of baseline blood parameters (hemoglobin, hematocrit and platelet count), comorbidities (arterial hypertension, diabetes mellitus, atherosclerosis) and antiplatelet use: these factors were then used as covariates in statistical analysis.
Results:
fMRI data analysis in the group of MPN patients revealed activation in the left primary sensorimotor cortex (pre- and post-central gyri); the right supramarginal gyrus showed significant activation (T = 5.99, pFWEcorr = 0.015) in the MPN group only. Group fMRI data analysis in healthy volunteers showed two main clusters of activation in the left precentral gyrus and right hemisphere of the cerebellum during task execution. Second-level analysis of activation differences between MPN patients and healthy volunteers showed greater activation in the right primary sensorimotor cortex in MPN (Puncorr = 0.014 and <0.001 at cluster and peak level respectively).
Conclusion:
Additional task-specific cortical activation in MPN patients may be potentially linked to NVU disturbance, even in otherwise unchanged cerebral activation patterns. Our findings also suggest that fMRI data in MPN may be confounded by higher blood cell count that needs to be controlled for in this cohort of patients.
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