%0 Journal Article
%T Differential blood-based biomarkers of subcortical and deep brain small vessel disease.
%A Hervella P
%A Alonso-Alonso ML
%A Sampedro-Viana A
%A Rodríguez-Yáñez M
%A López-Dequidt I
%A Pumar JM
%A Ouro A
%A Romaus-Sanjurjo D
%A Campos F
%A Sobrino T
%A Castillo J
%A Leira Y
%A Iglesias-Rey R
%J Ther Adv Neurol Disord
%V 17
%N 0
%D 2024
%M 38827243
%F 6.43
%R 10.1177/17562864241243274
%X UNASSIGNED: Cerebral small vessel disease is the most common cause of lacunar strokes (LS). Understanding LS pathogenesis is vital for predicting disease severity, prognosis, and developing therapies.
UNASSIGNED: To research molecular profiles that differentiate LS in deep brain structures from those in subcortical white matter.
UNASSIGNED: Prospective case-control study involving 120 patients with imaging-confirmed LS and a 120 control group.
UNASSIGNED: We examined the relationship between Alzheimer's disease biomarkers [amyloid beta (Aβ1-40, Aβ1-42)], serum inflammatory marker (interleukin-6, IL-6), and endothelial dysfunction markers [soluble tumor necrosis factor-like weak inducer of apoptosis, and pentraxin-3 (sTWEAK, PTX3)] with respect to LS occurring in deep brain structures and subcortical white matter. In addition, we investigated links between LS, leukoaraiosis presence (white matter hyperintensities, WMHs), and functional outcomes at 3 months. Poor outcome was defined as a modified Rankin scale >2 at 3 months.
UNASSIGNED: Significant differences were observed in levels of IL-6, PTX3, and sTWEAK between patients with deep lacunar infarcts and those with recent small subcortical infarcts (20.8 versus 15.6 pg/mL, p < 0.001; 7221.3 versus 4624.4 pg/mL, p < 0.0001; 2528.5 versus 1660.5 pg/mL, p = 0.001). Patients with poor outcomes at 3 months displayed notably higher concentrations of these biomarkers compared to those with good outcomes. By contrast, Aβ1-40 and Aβ1-42 were significantly lower in patients with deep LS (p < 0.0001). Aβ1-42 levels were significantly higher in patients with LS in subcortical white matter who had poor outcomes. WMH severity only showed a significant association with deep LS and correlated with sTWEAK (p < 0.0001).
UNASSIGNED: The pathophysiological mechanisms of lacunar infarcts in deep brain structures seem different from those in the subcortical white matter. As a result, specific therapeutic and preventive strategies should be explored.