Neurofeedback for insomnia: Current state of research.

BACKGROUND: Chronic insomnia affects about 6%-13% of the Canadian population. Although treatments already exist, they each have their own issues. Neurofeedback is a neuromodulation technique that specifically targets abnormal brain activity and is gaining attention as a possible insomnia treatment. AIM: To review the latest studies pertaining to the use of neurofeedback in the treatment of insomnia. METHODS: In this non-systematic review, only experimental studies assessing the effects of neurofeedback on patients with insomnia were targeted across four bibliographic databases. RESULTS: A total of 12 studies were retained. All neurofeedback studies included in this study showed a clear improvement of subjective sleep. However, data concerning objective improvement are contradictory. Most studies regarding surface and z-score neurofeedback show that neurofeedback targeting the sensorimotor rhythm in the sensorimotor cortex may help improve subjective sleep. A placebo effect seems also to be present in some studies. Several limitations were present in each study. CONCLUSION: While studies concerning neurofeedback as a treatment for insomnia are encouraging, many methodological barriers remain to be resolved to prove its efficacy unequivocally. More studies using robust design parameters, as well as the replication of existing studies, are necessary to support neurofeedback as an effective treatment for insomnia.

Inhibitory potential of chemical substitutions at bioinspired sites of ß-D-galactopyranose on neoglycoprotein/cell surface binding of two classes of medically relevant lectins.

Galactose is the key contact site for plant AB-toxins and the human adhesion/growth-regulatory galectins. Natural anomeric extensions and 3'-substitutions enhance its reactivity, thus prompting us to test the potential of respective chemical substitutions of galactose in the quest to develop potent inhibitors. Biochemical screening of a respective glycoside library with 60 substances in a solid-phase assay was followed by examining the compounds' activity to protect cells from lectin binding. By testing 32 anomeric extensions, 18 compounds with additional 3'-substitution, three lactosides and two Lewis-type trisaccharides rather mild effects compared to the common haptenic inhibitor lactose were detected in both assays. When using trivalent glycoclusters marked enhancements with 6- to 8-fold increases were revealed for the toxin and three of four tested galectins. Since the most potent compound and also 3'-substituted thiogalactosides reduced cell growth of a human tumor line at millimolar concentrations, biocompatible substitutions and scaffolds will be required for further developments. The synthesis of suitable glycoclusters, presenting headgroups which exploit differences in ligand selection in interlectin comparison to reduce cross-reactivity, and the documented strategic combination of initial biochemical screening with cell assays are considered instrumental to advance inhibitor design.