Memory Protection
Scientists analysed the way brain cells communicate at times of peake activity- such as the criation of new memories or seizures- when electrical signalling by the brain neurons are increased. They foun that GSK3 enzyme helps to supress brain activity by reducing the flow of chemical messengers bvetween brain cellss. This raises the possibility that drugs could be developed to block the effect of this enzyme, increasing chemical messaging between brain cells, researches say. This could help to protect memory in people with Alzheimer´s Disease and slow the progression of thier ilness. Conversely, researchers also say that drugs could also be developed to boost the efect of the enzyme, slowing brain activity in epilepsy patients and reducing the effects of their seizures , http://www.ed.ac.uk/news/all-news/alzheimers-110610.

The team of Dr Mike Cousin published an article in Nature Neuroscience and they found that theire results demonstrated a presynaptic role for GSK3 and they indicate that a protein kinase signaling cascade prepares synaptic vesicles for retrieval during elevated neruonal activity. Nature Neuroscience; jul2010, vol13 issue7 , p845-851.

Glycogen synthase kinase 3 (GSK3) was initially described as a key enzyme involved in glycogen metabolism, but is now known to regulate a diverse array of cell functions.
The study of the substrate specificity and regulation of GSK3 activity has been important in the quest for therapeutic intervention. However, our knowledge of the biological roles of GSK3 is still in its infancy, and much further experimentation is still necessary, exploiting the improved methodologies and reagents that are gradually becoming available. The development of increasingly potent and specific inhibitors of GSK3 will have an important
impact in helping to identify the true physiological substrates of GSK3, as will the availability of mice that lack either one or both GSK3 isoforms.
Philip Cohen and Sheelagh Frame