José María Frade. PhD
Scientific Director and Co-Founder
José María Frade.
Scientific Director. Founding Member
Researcher from the Instituto Cajal. Honorary Professor from the Madrid Universidad Autónoma.
José María Frade studied at the Madrid Universidad Complutense, where he graduated in Biological Sciences in 1989. Subsequently, he gained his doctorate in Science from the Madrid Universidad Autónoma in 1994. Between 1996 and 1998, he worked in Germany in the Neuro-biochemical Department of the Max-Planck Institute of Neurobiology. During this period he carried out studies on the induction of apoptosis mediated by the interaction of NGF with its receptor, p75NTR which were published in the prestigious scientific magazine Nature (Frade et al., 1996). At the end of 1998, Dr. Frade returned to Spain, to the Instituto Cajal, where he continued with his studies on apoptosis caused by HGF and its relation to the activation of the cell cycle in neurons. In August of 2000, Dr. Frade obtained a place as a Senior Scientist at the Instituto Cajal and in July, 2008 he became a Scientific Researcher at the same Institute. Currently, he leads a research group that is studying the mechanisms involved in the activation of the cell cycle in neurons and the neuronal tetraploidisation in the normal and pathological brain (Morillo et al., 2010). As a result of this work, Dr. Frade has been able to demonstrate that the phosphorylation of the molecule E2F4 is crucial for the generation of tetraploid neurons (Morillo et al., 2012), which increase in number in the brains of Alzheimer patients. Consequently, Dr. Frade has patented the blocking of the phosphorylation of E2F4 as a possible therapy for Alzheimer’s disease, a patent that has been licensed by Tetraneuron, S.L. Work carried out in recent years has confirmed the pathological role of the aforementioned phosphorylation in Alzheimer model animals. Currently, Dr. Frade is actively working on the development of a drug that can be used to prevent the neuronal tetraploidisation and the consequent cognitive loss in Alzheimer’s disease.