Dr. Alberto Pascual joined the Instituto de Biomedicina de Sevilla (IBiS, Spain.) in 2011. He obtained his PhD degree at the University of Seville and moved to the laboratory of Prof. Thomas Preat for a postdoctoral stage in France at CNRS, studying learning and memory. His career has been centred in neurodegeneration and more recently his main interest has become modifiable risk factors in AD. AD is characterised by a pathognomonic early decrease in brain blood flow, the accumulation of Aß peptide in the wall of brain vessels (amyloid angiopathy), and high local inflammation surrounding senile plaques. These three circumstances lead to a decrease in oxygen concentration that could modify the progression of AD. We have shown that the human AD brain shows molecular markers of hypoxia and the accumulation of HIF1alpha in Aß plaque-associated microglia of AD mouse models. Low oxygen levels disrupt mitochondrial activity of microglia, leading to cell cycle arrest and worsening AD pathology in animal models of AD. Actually, we are investigating the role of local hypoxia in the angiogenic processes taking place around Aß plaques. We have described a new structure associated with amyloid deposits that we have named vascular scars (VaS). VaS are complexes endothelium-derived structures characterised by low perfusion and high extracellular matrix accumulation, mimicked by endothelial loss of function mutations in PSEN1/2, and generated by non-productive angiogenesis and the activity of microglia.