Since I graduated, I have being working on two main topics: the study of neurodegenerative processes and its relationship with adult neurogenesis (a component of the cognitive reserve). During my PhD, at the University of Salamanca (Spain) under the supervision of Dr J.R. Alonso and Dr E. Weruaga I collaborated with the laboratory of Dr. M. Lafarga and Dr. M. Berciano (University of Cantabria, Spain) identifying nuclear markers of pre-degeneration in the Purkinje cell degeneration (pcd) mice. This was a multidisciplinary study done in collaboration with other institutions which resulted in the publication of a patent and established the basis for further works. Moreover, on my PhD work at Salamanca I optimized a protocol to detect proliferating cells in brain tissue and I demonstrated that the degeneration of mitral cells affects migration and survival of new neurons in the olfactory bulb, while collaborating in other works about olfactory bulb plasticity. I continued my studies on the relationship between adult neurogenesis and neurodegeneration at King’s College of London (at The Pediatric Storage Disorders Lab, UK) analyzing, under the supervision of Dr J. Cooper, adult neurogenesis in animal models and human samples of Batten's disease (an infantile neurodegenerative disease). Then, I moved to Barcelona and worked at the laboratory of Dr. C. Saura in the Institute for Neuroscience (Universitat Autónoma de Barcelona, Spain), where I developed a project demonstrating that cognitive stimulation is able to revert memory deficits and recover normal hippocampal neurogenesis in an animal model of AD. At the same time, I was highly involved in other projects on molecular aspects of AD and also Huntington’s disease. In particular, I analyzed microarray data, optimized a protocol for intracranial delivery of adeno-associated viral vectors to overexpress the CREB-regulated transcription coactivator 1 (CRTC1) in the hippocampus (which resulted on memory improvement in an AD mouse model). Our work revealed an important role of CRTC1 in the control of transcriptional patterns associated to memory function in AD. During the last two years I have been working at the laboratory of Neuroprotection and Neurogenesis in Brain Repair (Center for Neuroscience and Cell Biology, CNC, University of Coimbra, Portugal) under the supervision of Dr. J. Malva and I have carried out a project demonstrating that systemic inflammation is able to affect, at the mid/long-term, some components of the cognitive reserve (adult neurogenesis, size of dendritic tree and number of synaptic puncta) and impair memory capacities (measured by using Morris Water Maze test, MWM) in wild type and the triple transgenic mouse model of AD (paper under submission). Therefore, I have become highly interested on the effects of inflammation and microglial function on adult neurogenesis and memory (4). Furthermore, at the CNC I have collaborated with other members of the center analyzing adult neurogenesis in vitro and in vivo and established collaborations abroad aimed to analyze effects of NPY in memory and dendritic growth, the efficacy of gene therapy on a rat model of temporal epilepsy and characterize a new animal model of temporal epilepsy. During the last year I have also developed some automated systems for image analysis (based on ImageJ macro programming) to estimate the volume of brain regions, the number of synaptic puncta, to quantify immunofluorescence staining in brain slices and track mouse paths in the MWM.