Emerging Roles of microRNAs in Ischemic Stroke: As Possible Therapeutic Agents / 대한뇌졸중학회지

Stroke is one of the leading causes of death and physical disability worldwide. The consequences of stroke injuries are profound and persistent, causing in considerable burden to both the individual patient and society. Current treatments for ischemic stroke injuries have proved inadequate, partly owing to an incomplete understanding of the cellular and molecular changes that occur following ischemic stroke. MicroRNAs (miRNA) are endogenously expressed RNA molecules that function to inhibit mRNA translation and have key roles in the pathophysiological processes contributing to ischemic stroke injuries. Potential therapeutic areas to compensate these pathogenic processes include promoting angiogenesis, neurogenesis and neuroprotection. Several miRNAs, and their target genes, are recognized to be involved in these recoveries and repair mechanisms. The capacity of miRNAs to simultaneously regulate several target genes underlies their unique importance in ischemic stroke therapeutics. In this Review, we focus on the role of miRNAs as potential diagnostic and prognostic biomarkers, as well as promising therapeutic agents in cerebral ischemic stroke.

Effect of Gallic acid on dementia type of Alzheimer disease in rats: electrophysiological and histological studies

Introduction: To study the effect of gallic acid [GA] on hippocampal long-term potentiation [LTP] and histological changes in animal model of Alzheimer disease [AD] induced by beta-amyloid [Abeta]

Methods: Sixty-four adult male Wistar rats [300 +/- 20 g] were divided into 8 groups: 1] Control [Cont]; 2] AD; 3] Sham; 4-7] AD+GA [50, 100, and 200 mg/kg for 10 days, orally] or vehicle, 8] Cont+GA100, Abeta [1microg/microL in each site] was infused into hippocampus bilaterally. Changes of amplitude and slope of LTP induced in hippocampal dentate gyrus [DG] were evaluated by high frequency stimulation [HFS] of perforant path [PP]

Results: Data showed that LTP amplitude and area under curve significantly impaired in AD rats [P<0.001], while significantly improved in AD rats treated with GA [P<0.05, P<0.01]

Conclusion: Current findings suggest that GA reduces neural damage and brain amyloid neuropathology and improves cognitive function via free radicals scavenging and inhibiting oligomerization of Abeta but with no effect on healthy rats