Our research focuses on understanding adult hippocampal neurogenesis (AHN), which involves the generation of new neurons in the brain's hippocampus. AHN plays a crucial role in learning, mood regulation, and the integration of new neurons. We investigate AHN's role in both normal aging and neurodegenerative diseases like Alzheimer's, ALS, Parkinson's, and more. Our recent findings revealed AHN's persistence in human aging and its impairment in neurodegenerative conditions.

Mitochondria are intricate organelles with vital metabolic roles in cells. Our lab concentrates on defects in the oxidative phosphorylation system caused by mitochondrial mutations linked to diseases. We investigate how these dysfunctions impact cellular health and metabolic processes, aiming to comprehend their effects on conditions such as neurodegeneration and diabetes. Our long-term goal is to develop therapies based on this knowledge.

Our lab investigates how gender-based metabolic differences, particularly involving mitochondria, impact health and disease. We're focusing on two main projects: one related to metabolism and another to cardiovascular disease. In the metabolism project, we're studying how mitochondria vary between sexes and their role in physiological differences. For cardiovascular disease, we're exploring gender-related mitochondrial disparities during heart failure progression. Our goal is to identify potential therapeutic targets for heart failure.

Our group focuses on understanding the cellular and molecular mechanisms that control T-cell lineage commitment and differentiation in the human thymus. We aim to uncover how dysregulation of these mechanisms contributes to T-cell acute lymphoblastic leukemia (T-ALL), with the goal of identifying therapeutic targets. Our research primarily centers on the NOTCH1 pathway, a major driver of T-ALL. We have developed innovative models to study human T-ALL and have utilized this knowledge to develop targeted therapies, such as CAR-T cells and antibody-drug conjugates.

During 2021 and 2022, our research focused on: (i) further studying the role of the SLAMF1 immune receptor in Trypanosoma cruzi infection and identifying therapeutic target genes; (ii) assessing the prognostic value of the TCFL5 isoform sCha in Chagas disease patients; (iii) investigating cardiac remodeling in T. cruzi infection; (iv) exploring the mitochondrial genome, transcriptome, and proteome of T. cruzi. We also found autoantibodies predicting sudden death risk in Chagas cardiomyopathy and collaborated on TCFL5 studies in spermatogenesis and colorectal cancer with Dr.

The African swine fever virus (ASFV) is a complex pathogen that affects pigs and wild boars, threatening the global pork industry. Our group investigates how the virus evades the host immune response and aims to develop an effective vaccine. We have discovered that certain genes of the virus are linked to its ability to counteract the immune response. We are developing live attenuated vaccines that have proven to be safe and protective in pigs, which could be key in controlling the spread of the virus.

Our research line is mainly focused on the study and characterisation of macroscopic and histopathological lesions, pathogenic mechanisms, inflammatory and immune response in animal infectious diseases, with special attention to emerging and re-emerging diseases that may affect production and free-living animals such as African swine fever or bluetongue, and zoonoses with public health implications such as Rift Valley fever or SARS-CoV-2.

We examine the role of genetic and non-genetic inheritance, the role of the environment as a phenotypic inducer through epigenetic regulation, and the possibility that such epigenetic changes may evolve under selection towards accommodated genetic variation. We delve into the natural history of species, populations, and communities to study interactions between species, identify functional polymorphisms in candidate genes to explain ecologically and evolutionarily divergent life history traits, and evaluate the genomic basis of fitness reductions in endangered species.