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Este trabajo fue presentado como comunicación tipo póster en el citado congreso. Objectives: Review of the published literature concerning the relationship between microbiome and gastrointestinal cancer. Methods: Present work is focused on systematic research in the most prominent biomedical databases finds relevant works in Pubmed and the library’s catalog of the University of Málaga (Jábega) of published journals in the last 5 years. Results: In this work, the mechanisms used by the microbiome to damage gastrointestinal epithelial cells and cause cancer are explained. Some of them are the dysbiosis, destruction of the mucosal barrier, chronic inflammation, damage caused by metabolites produced in the digestion and the direct attack of certain toxins to the cell’s DNA. These mechanisms adjust the immune response, by activation or inhibition using different cytokines. There is also a deeper look into several microorganisms and how they cause gastrointestinal cancer using toxins or virulence factors to activate them. Conclusions: The evidence found so far about the microbiota and gastrointestinal cancer is enough to assume the relationship between them, although there is much left to research. With these findings, it can be expected that in a near future certain microorganisms could be used for screening purposes, due to their increase in early stages of the tumor genesis and also, in a preventive way to try to eradicate them, even avoid cancer. Studies on the microbiota are hardly beginning, and results appear to be promising. Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech.

Alzheimer's disease (AD) constitutes the most prevalent form of dementia. There is no cure so there is an urgent need of novel therapeutic targets and treatments. The main histopathological hallmarks of AD brains are extracellular plaques formed by the beta-amyloid (Abeta) peptide, and intraneuronal neurofibrillary tangles composed of hyperphosphorylated tau (phospho-tau). In fact, AD is considered a neurodegenerative proteinopathy. The coexistence of these protein aggregates leads to synaptic damage, neuronal loss and cognitive decline in patients. The dysfunction of intracellular proteolytic systems (autophagy-lysosomal and ubiquitin-proteasome) has been postulated as a pathological mechanism contributing to the cerebral accumulation of these toxic proteins. Our aim is to verify the involvement of these pathways in the hippocampus of two different transgenic mice of AD to understand the differential impact of Abeta and phospho-tau accumulation on the pathological progression. Cerebral sections from APP/PS1 and ThyTau22 models (2 to 18 months) were analyzed. WT animals were used as controls. Immunohistochemical stainings were performed to evaluate amyloid deposition, phospho-tau accumulation, autophagic/lysosomal markers and ubiquitin at different pathological stages. In the amyloidogenic model we found a pathological accumulation of autophagic vesicles, lysosomes and ubiquitin in periplaque dystrophic neurites. In ThyTau22 model, only abnormal accumulation of ubiquitin was detected. These results demonstrate significant alterations of the proteolytic pathways in both models of proteinopathy even though they were differentially affected. Preclinical studies in transgenic models able to reproduce the pathogenic mechanisms of patients will allow the identification of novel therapeutic targets and to test effective treatments. Compounds able to reduce the burden of toxic proteins might be an alternative pharmacological approach to AD and other tauopathies. Supported by CTS-429 (Biology and Histology), and Instituto de Salud Carlos III (ISCiii) of Spain, co-financed by FEDER funds from European Union through grant PI21/00915 (to AG). Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech.

Introduction: During both obstructive congenital hydrocephalus and post-hemorrhagic hydrocephalus additional pathological events are intimately associated with their ethiology: a) a detrimental inflammatory response; b) severe damage of the underlying periventricular nervous tissue, including white matter, and c) damage on the ventricular wall. Therapeutic approaches have been directed to overcome a) and b), however recovery of damaged neuroepithelium/ependyma is, in our present, an important therapeutic gap. Methods: Human and mouse induced pluripotent stem cells (iPSC) have been artificially differented into ependymal progenitors. Intracerebroventricular (ICV) injections of iPCS are performed ex vivo and in vivo in the damaged ventricular wall. Their integration and differentiation has been studied by immunohistochemistry and histopathological analysis. Also, the effect of TNF-alpha on the recovery of the ventricular wall will be tested. Results: Mice and human ependymal progenitors are able to integrate and differentiate into ependyma in damaged ventricular wall. Stage of ependymal differentiation by the time of the injection defined different degrees of integration. Conclusions: iPSC appear to be a good ependymal progenitor source with no ethical controversy associated. Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech.

Comunicación oral. El resumen no se publica por deseo de los autores NG2 cells are considered oligodendrocyte precursor cells (OPC). In pathological conditions, NG2 cells contribute to generate oligodendrocytes and reactive astrocytes. This study has been designed to uncover the role of NG2 cells in congenital hydrocephalus using the hyh mouse model. Materials and methods Brain sections and whole mount preparations were obtained from embryos and postnatal hyh and control mice. NG2 positive (NG2+) cells were co-labelled with different IHC markers to deepest identification. Additionally, trying to understand reproducibility of our results in different neurodegenerative conditions, same NG2 identification approach was performed using ventricular walls explants from control mice after mechanical induction of astrocyte reaction. Results A higher number of NG2+ cells were found in the hyh mice compared to the control mice. In addition, NG2+ cells in the hyh mice showed a higher NG2 antigen content compared to the control mice. In the hyh mouse, colocalization results showed that most of NG2+ cells were identified as OPC cells and pericytes, but never as reactive astrocytes o microglial cells. However, in the same approach performed in neurodegenerative conditions, NG2+ cells were mostly identified as reactive astrocytes. Conclusions NG2 progenitors appear to be affected in hyh mutant mice giving rise to a different NG2+population which role in hydrocephalus is still unkown. Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech.