Mild Cognitive Impairment and Neurofeedback: A Randomized Controlled Trial.

Mild cognitive impairment (MCI) is often a precursor of dementia, and in particular of Alzheimer's Disease (AD) which is the most common cause of dementia. Individuals with amnestic MCI are several-fold more likely to develop AD than the general population. Therefore, MCI comprises a well-detectable, early stage time-point for therapeutic intervention and strategic prevention.

Assisted reproductive technology and long-term ophthalmic morbidity of the offspring.

In this study, we investigate if children born following assisted reproduction technologies (ARTs) are at an increased risk for long-term ophthalmic complications. For this purpose, a population-based cohort analysis was conducted which included all deliveries between 1991 and 2014 at a single tertiary medical center. Offspring were classified relative to conception method as ART or spontaneous pregnancies.

Neurofeedback Improves Memory and Peak Alpha Frequency in Individuals with Mild Cognitive Impairment.

Mild cognitive impairment (MCI) is a syndrome characterized by a decrease in cognitive abilities, while daily function is maintained. This condition, which is associated with an increased risk for the development of Alzheimer's disease, has no known definitive treatment at present. In this open-label pilot study we explored the possible benefits of neurofeedback for subjects with MCI.

Synapsin selectively controls the mobility of resting pool vesicles at hippocampal terminals.

Presynaptic terminals are specialized sites for information transmission where vesicles fuse with the plasma membrane and are locally recycled. Recent work has extended this classical view, with the observation that a subset of functional vesicles is dynamically shared between adjacent terminals by lateral axonal transport. Conceptually, such transport would be expected to disrupt vesicle retention around the active zone, yet terminals are characterized by a high-density vesicle cluster, suggesting that counteracting stabilizing mechanisms must operate against this tendency.

Inhibition of exocytosis or endocytosis blocks activity-dependent redistribution of synapsin.

The synaptic vesicle cycle encompasses the pre-synaptic events that drive neurotransmission. Influx of calcium leads to the fusion of synaptic vesicles with the plasma membrane and the release of neurotransmitter, closely followed by endocytosis. Vacated release sites are repopulated with vesicles which are then primed for release.