[Clustering of diagnostic MRI signs of cerebral microangiopathy and its relationship with markers of inflammation and angiogenesis].

Autor:	Dobrynina LA; Research Center of Neurology, Moscow, Russia., Gnedovskaya EV; Research Center of Neurology, Moscow, Russia., Zabitova MR; Research Center of Neurology, Moscow, Russia., Kremneva EI; Research Center of Neurology, Moscow, Russia., Shabalina AA; Research Center of Neurology, Moscow, Russia., Makarova AG; Research Center of Neurology, Moscow, Russia., Tzipushtanova MM; Research Center of Neurology, Moscow, Russia., Filatov AS; Research Center of Neurology, Moscow, Russia., Kalashnikova LA; Research Center of Neurology, Moscow, Russia., Krotenkova MV; Research Center of Neurology, Moscow, Russia.
Jazyk:	ruština
Zdroj:	Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova [Zh Nevrol Psikhiatr Im S S Korsakova] 2020; Vol. 120 (12. Vyp. 2), pp. 22-31.
DOI:	10.17116/jnevro202012012222
Abstrakt:	Objective: To perform cluster analysis of MRI signs of cerebral microangiopathy (small vessel disease, SVD) and to clarify the relationship between the isolated groups and circulating markers of inflammation and angiogenesis. Material and Methods: The identification of groups of MRI signs (MRI types) using cluster hierarchical agglomerative analysis and iterative algorithm of k-means and assessment of their relationship with serum concentrations of tumor necrosis factor-α (TNF-α), transforming growth factor-β1 (TGF-β1), vascular endothelial growth factor-A (VEGF-A), hypoxia-inducible factor 1-α (HIF1-α) determined by ELISA were performed in 96 patients with SVD (STRIVE, 2013) (65 women, average age 60.91±6.57 years). Results: Cluster analysis of MRI signs identified two MRI types of SVD with Fazekas grade 3 of white matter hyperintensity (WMH). MRI type 1 ( n =18; 6 women, mean age 59.1±6.8 years) and MRI type 2 ( n =22, 15 f., mean age 63.5±6.2 years) did not differ by age, sex, severity of hypertension, presence of other risk factors. MRI type 1 had a statistically significantly more pronounced WMH in the periventricular regions, multiple lacunes and microbleeds, atrophy, severe cognitive impairment and gait disorders compared with MRI type 2. Its formation was associated with a decrease in VEGF-A level. MRI type 2 had the significantly more pronounced juxtacortical WMH, white matter lacunes, in the absence of microbleeds and atrophy, and less severe clinical manifestations compared with MRI type 1. Its formation was associated with an increase in TNF-α level. Conclusion: Clustering of diagnostic MRI signs into MRI types of SVD with significant differences in the severity of clinical manifestations suggests the pathogenetic heterogeneity of age-related SVD. The relationship of MRI types with circulating markers of different mechanisms of vascular wall and brain damage indicates the dominant role of depletion of angiogenesis in the formation of MRI type 1 and increased inflammation in the formation of MRI type 2. Further studies are needed to clarify the criteria and diagnostic value of differentiation of MRI types of SVD, and also their mechanisms with the definition of pathogenetically justified prevention and treatment of various forms of SVD.
Databáze:	MEDLINE
Externí odkaz:	Zobrazit plný text záznamu