Therapeutic strategies to prevent or delay neurodegenerative diseases and loss of synapses due to diseases or normal aging based on gene therapy or on compounds activating PI3K

BACKGROUND

The number of synapses is a major determinant of cognitive abilities. Aging and certain brain diseases cause gradual synapses loss accompanied of mental decline. We have shown that this loss and consequent mental decline might be prevented or delayed by stimulation of the enzyme phosphoinositide 3 kinase (PI3K) independently of age. PI3K is an enzymatic family involved in the signalling cascade in cell proliferation, differentiation, chemotaxis and survival.

TECHNOLOGY

Treating human neuroblastoma cells with the synthetic peptide 740Y-P (previously shown to translocate across the membrane of intact cells and activate PI3K) we have demonstrated that activity of PI3K controls the expression and localization of synaptic markers. These results are backed by our findings in Drosophila, showing that both PI3K activation and over-expression result in the formation of new synapses in larvae, adult and aged adult neurons. These new synapses require the continuous activity of PI3K.  

We propose to develop therapeutic strategies to prevent or delay neurodegenerative diseases and loss of synapses due to diseases or normal aging. Such strategies may be based on gene therapy approaches or on compounds activating PI3K.

PCT (International) patent application filed

Pharmaceutical or biotechnological companies interested in screening compounds capable of preventing loss of neural synapses during aging or disease-related neurodegeneration by activating the enzyme phosphoinositide 3 kinase.

A patent licensinsg approach with technical cooperation is offered