5^th International Conference on Alzheimer’s Disease & Dementia September 29-30, 2016 London, UK

Claude M Wischik holds the Chair in Old Age Psychiatry at the University of Aberdeen in Scotland, and is Executive Chairman of TauRx Pharmaceuticals. He studied medicine in Australia, completed his PhD at the Laboratory of Molecular Biology in Cambridge, and also higher psychiatric training in Cambridge. He was the first to identify Tau protein as the main constituent of the Alzheimer tangle and developed the first Tau Aggregation Inhibitors. He has published 121 papers and holds 11 patent groups based on his work with over 40 individual patents.

Jerzy Leszek is Professor of Psychiatry, Vice-Head of the Department of Psychiatry and Head of Alzheimer’s Disease Lab at the Medical University in Wroclaw, Poland. He graduated at Medical University of Wroclaw in 1979, was awarded a doctorate in Wroclaw in 1981 and in 1999- examination for the degree of associate professor of psychiatry and since 2007 he is working as full professor of psychiatry at Wroclaw Medical University. He is author and co-author more than 280 papers (especially from old age psychiatry), some chapters to the books published in reputed Polish and international journals and serving as an editorial board member of several journals.

The lack of effective treatment for Alzheimer’s disease(AD) stems mainly from the incomplete understanding of AD causes. Currently there are several hypotheses which try to explain the early molecular mechanisms of AD pathogenesis. Nanomedicine as a biomedical and pharmaceutical application of nanotechnology for making nanocarriers like dendrimers has shown great potential for the treatment of many CNS diseases. Dendrimers are polymeric molecules chemically synthesized with well defined shape size and nanoscopic physicochemical properties reminiscent of proteins. Recently an increasing number of studies have been focused on the potential of dendrimers to prevent aggregation and fibrillation of proteins involved in neurodegenerative disorders such as AD. Some of dendrimers were demonstrated to cross blood-brain barrier, which legitimized research on these compounds as potential drugs for neurological disorders. Recent our studies have revealed that dendrimers possess the intrinsic ability to localize in cells associated with neuroinflammation(activated microglia and astrocytes) and thus can be used as drug carriers in neuroinflammation therapy. Above/mentioned findings may be of high significance in the context of potential application of dendrimers as drug carriers or active compounds per se. According to the opinion the author’s of this presentation ,they are promising macromolecules for further investigations on their applicable in neurodegenerative disorders , for instance AD.

Jordan L. Holtzman, M.D., Ph.D. is Professor, Departments of Pharmacology and Medicine and Division of Environmental Health Sciences, University of Minnesota, Minneapolis, USA. He was graduated from University of Chicago, the Pritzker School of Medicine in 1959. He completed internship from University Ill Rsc/Ed in 1960.

Alzheimer’s disease is described as a progressive dementia associated with the extracellular deposits in the brain of a garbage protein, β-amyloid (Aβ), and the intracellular deposits of tangles. The vast majority of the patients develop the disease in old age while a small portion have an early onset, familial form. Since the 1970’s it has been generally assumed that the dementia seen in the two forms is due to the neurotoxicity of the Aβ. With the purification and sequencing of Aβ in the 1990’s investigators were able to identify the mutations associated with the familial forms. A number of laboratories transfected mice with these mutated genes. Since these animals exhibited many of the pathological and clinical manifestations of the late onset disease, they have been used to screen for new therapeutic agents. Unfortunately, all 244 drugs identified in these models have failed in clinical trials in elderly patients. Work from my laboratory has suggested that plaque deposits of Aβ rather than causing the dementia is merely a biomarker for a decline in the capacity of the endoplasmic reticulum (ER) in the cells to catalyze the posttranslational processing of 40% of cellular proteins, including those synaptic, membrane proteins required for a functioning memory. This paradigm is based on our observation that in the CSF all Aβ is normally N-glycosylated and bound to ER proteins, ERp57 and calreticulin. These data suggest a new direction for drug discovery in which agents are screened for their ability to increase the levels in cell lines of fluorescently labeled components of the ER post-translational pathway. The development of these cell lines would permit rapid screening for potential therapeutic agents in plate readers.