Gsk3 enzyme is one of the most interesting protein.  In Jope's paper about it, he showed us the caracteristic that gsk3 has of change it's way to work depending of the place that it is. If it is in the cytosolic compartiment it acts phosphorylating proteins that become active or inactive. If it is in the nucleus it acts in growing factors. Sometime thies enzyme is present in mithocondrias and acts in a survive or apoptotic way.
About this you can read Jope,2004.

We have a research group called GPNF in UNiversity of Faculdade de Ciências Médicas da SanTa Casa de São Paulo in São Paulo , Brazil. Our group studies Alzheimer's Disease and lithium in this disease. Our sponser Hudson Buck speake in a television program about our researches.
This speake is in this link http://www.youtube.com/watch?v=aObuymgo_3Q .

There is a lot of papers now a days presenting energy deficits as a mainly mecahanism in Alzheimer's Disease.
In these pathway our GSK3 always is present.
One of this papers is Tau Phosphorylation by GSK3 in Different Conditions, wroten by Jesús Avila et al,  in International Journal of Alzheimer’s Disease Volume 2012.
Evere day I have a huge surprise about this enzyme.

There is a new paper about GSK3 and cardiac muscle: Cross-talk between glycogen synthase kinase β (GSK3β) and p38MAPK regulates myocyte enhancer factor 2 (MEF2) activity in skeletal and cardiac muscle. Dionyssiou MG, Nowacki NB, Hashemi S, Zhao J, Kerr A, Tsushima R, McDermott JC.
This is an intereasting paper and they citated our paper abou Lithium and Alzheimer´s disease.
Microdose lithium treatment stabilized cognitive impairment in patients with Alzheimer�s disease.
Both are in Pubmed.

Lithium and GSK-3 beta enzyme

We published an article in Current Alzheimer Research about treating Alzheimer´s Disease with Lithium Microdose. Look at http://www.ncbi.nlm.nih.gov/pubmed/22746245. I want to talk with other researchers about Lithium and GSK-3beta enzyme.

There is an article in Neuron magazine published in 2007 that conclude that We conclude that the regulation of GSK3b activity provides a powerful mechanism to preserve information encoded during LTP from erasure by subsequent LTD, perhaps thereby permitting the initial consolidation of learnt information.

During LTD, activation of PP1 leads to dephosphorylation of GSK3b at ser9 to further activate GSK3b and enable LTD to occur. PP1 also inhibits Akt. During LTP, activation of NMDA receptors leads to stimulation of the PI3K-Akt pathway, which phosphorylates GSK3b at ser9 to inhibit its activity and prevent the induction of LTD. Thus, GSK3b, under the control of Akt and PP1, is a critical determinant of the direction of NMDA receptor-dependent plasticity.

Stéphane Peineau et col. A Role for GSK3b in Synaptic Plasticity

Neuron 53, 703–717, March 1, 2007

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.