Bajic Vladan, PhD,VMD Celjska 7  Belgrade,Serbia  (381) 113610314  vladanbajic@yahoo.com PROFESSOR OF RESEARCH FULBRIGHT ALUMNI Education Belgrade UNIVERSITY – School of Veterinary Medicine, Belgrade, Serbia PhD in Genetic toxicology, 2002 MS in Genetic toxicology, 1998 Doctor of Veterinary Medicine Experience Galenika Pharmaceutical Company, Institute for Pharmaceutical Research, Biomedical Department, COMPANY (one of the top 3 pharmaceutical manufacturers in Serbia) – Belgrade, Serbia Research Scientist, 1992 to 2003, and from 2007 to present Expert Associate for genetics and neurotoxicology Professor of Research, Neurosciences (2012) Managerial posts, 2003-2006 Assistant to General Manager for R&D, Galenika pharmaceuticals Director of Biomedical Research Institute, Galenika pharmaceuticals Member of board of Directors Galenika a.d. Member of the Board of Directors, Velefarm (pharmaceutical distribution company) Research Fellowship Fulbright Scholar; Assistant Professor of Research Case Western University, Department of Pathology, School of Medicine 2103 Cornell Road, Ceavland, Oh 44106, USA DAAD Scholar, Germany, Leipzig Medical University, Institute for Brain Research The Fulbright Scholar Grant (2008) and DAAD grant (2011) and with collaboration from Prof dr Mark A Smith and Prof dr Thomas Arendt I have produced to date several peer-reviewed publications and conference appearances from each project. My research activity was mainly concentrated on multi-level expression patterns of late core cell cycle associated proteins that are subjected to a specific chromosomal instability phenotype in Alzheimer’s disease, i.e. the cell cycle re entry phenotype and its relation to APP processing and Abeta. Interested In: Addressing the issue of X chromosome instability in AD of women and the notion to address X inactivation patterns in the AD brain as we have found that the X chromosome is indeed not stable, shows premature centromere separation, a centromere instability syndrome that may have more profound effect in the interphase neuron than we expect (changes in chromosomal territory architecture). We are now in the process of looking into the methylation status of the X chromosome in AD patients (LOAD) and age matched controls in order to define is their any skewing. Also, due to the facts that X chromosome instability may express centromere/cohesion instability in neurons and peripheral blood lymphocytes, possibly as a result of faulty cell cycle re entry of vulnerable neurons, we are also looking at late core cell cycle proteins (APC/c, CDK 11, MAD2, MAD2b, BUbR1, securin and other..) and their relationship with APP processing and Abeta. Most of these proteins have other roles in the interphase neurons other than their cell cycle roles and are expressionaly changed in Alzheimer’s disease. Hopefully, I will have cooperation with other labs in order to tackle these questions...in a deeper and more profound way...