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The MoCA is superior to the MMSE in the detection of patients with cognitive impairment at higher risk for incident dementia at a memory clinic setting.

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Brief screening tests during acute admission in patients with mild stroke are predictive of significant vascular cognitive impairment 3-6 months after stroke.

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Considerable evidence suggests that depression is related to interhemispheric functional coordination deficits. For depression, electroconvulsive therapy (ECT) is the most rapid and effective therapy, but its underlying mechanism remains unknown. The aim of this study was to explore the impact of ECT on the interhemispheric functional coordination in depression patients. We used resting-state functional magnetic resonance imaging to observe the change of interhemispheric functional coordination with the method of voxel-mirrored homotopic connectivity (VMHC) in 11 depressed patients before and after ECT, compared with 15 healthy controls. The results showed that, compared with depression patients before ECT, VMHC was significantly increased in superior frontal gyri (BA 8), middle frontal gyri (two clusters: BA 8/9 and BA 10) and angular gyri (BA 39) in depression patients after ECT. Compared with healthy controls, VMHC in those areas was significantly lower in the middle frontal gyri (BA 8/9) and angular gyri (BA 39) in depression patients before ECT, but no significant difference was observed in the superior frontal gyri (BA 8) and middle frontal gyri (BA 10). There was no significant correlation between the changes of Hamilton Depression Rating Scale scores and changed VMHC values in those four areas in depression patients. The results suggest that ECT selectively modulated interhemispheric functional coordination in depression patients. Such may play an important mechanistic role in the treatment of depression, and may afford a useful avenue for optimizing treatment.

Cysteinyl leukotrienes (CysLTs) are potent inflammatory mediators that predominantly exert their effects by binding to cysteinyl leukotriene receptors of the G protein-coupled receptor family. CysLT receptor 2 (CysLT 2 R), expressed in endothelial cells of some vascular beds, has been implicated in a variety of cardiovascular functions. Endothelium-specific overexpression of human CysLT 2 R in transgenic mice (hEC-CysLT 2 R) greatly increases myocardial infarction damage. Investigation of this receptor, however, has been hindered by the lack of selective pharmacological antagonists. Here, we describe the characterization of 3-(((3-carboxycyclohexyl)amino)carbonyl)-4-(3-(4-(4-phenoxybutoxy)phenyl)-propoxy)benzoic acid (BayCysLT 2 ) and explore the selective effects of this compound in attenuating myocardial ischemia/reperfusion damage and vascular leakage. Using a recently developed ␤-galactosidase-␤-arrestin complementation assay for CysLT 2 R activity (Mol Pharmacol 79: 270-278, 2011), we determined BayCysLT 2 to be ϳ20-fold more potent than the nonselective dual CysLT receptor 1 (CysLT 1 R)/ CysLT 2 R antagonist 4-(((1R,2E,4E,6Z,9Z)-1-((1S)-4-carboxy-1-hydroxybutyl)-2,4,6,9-pentadecatetraen-1-yl)thio)benzoic acid (Bayu9773) (IC 50 274 nM versus 4.6 M, respectively). Intracellular calcium mobilization in response to cysteinyl leukotriene administration showed that BayCysLT 2 was Ͼ500-fold more selective for CysLT 2 R compared with CysLT 1 R. Intraperitoneal injection of BayCysLT 2 in mice significantly attenuated leukotriene D 4 -induced Evans blue dye leakage in the murine ear vasculature. BayCysLT 2 administration either before or after ischemia/reperfusion attenuated the aforementioned increased myocardial infarction damage in hECCysLT 2 R mice. Finally, decreased neutrophil infiltration and leukocyte adhesion molecule mRNA expression were observed in mice treated with antagonist compared with untreated controls. In conclusion, we present the characterization of a potent and selective antagonist for CysLT 2 R that is useful for discerning biological activities of this receptor.

Our findings support a vascular contribution to neurodegeneration and cognitive impairment.