We describe the development of a mouse model for a human polymorphism in the serotonin transporter linked to increased anxiety
My research
A review of epigenetic mechanisms in cognitive and neurodegenerative diseases.
In my PhD thesis, I described the role that several molecules within the signalling cascade that activates the transcription factor CREB (cAMP Response Element Binding protein) play in long-term memory formation. In humans and mice, mutations in the genes encoding for several proteins within such molecular cascade result in learning and memory deficits. Awarded an Extraordinary Doctorate Award.
A new mechanism by which environmental enrichment triggers enhanced learning and memory in mice.
Here we validate a new mouse model for a rare human disease called Rubinstein-Taybi syndrome, characterized by skeletal malformations and intellectual disability.
We discover that an increase of neuronal excitability, triggered by enhanced activity of the transcription factor CREB, boosts simple forms of associative memory.
Contrary to what would be expected of a molecular intermediary of memory formation, we find that increased levels of CREB activity lead to deficits in some forms of complex memory that involve fine spatial mapping and navigation. We conclude that a balanced level of CREB activity is a requisite for optimal learning.
Here we describe the deficits of learning and other behavioural anomalies in a mouse model for a rare disease associated with intellectual disability called Costello syndrome.
A short review of some of the neural plasticity mechanisms that underlie memory formation and, in particular, those molecular processes that allow for a restricted set of synapses within the neuron to be selected and ‘tagged’ to undergo the modifications that sustain long-term memory of specific stimuli and experiences. Published in the prestigious ‘Journal of Neuroscience’.