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Under the leadership of Dr. Judes Poirier, C.Q., ADGEN is a multidisciplinary research unit  dedicated to the understanding of the molecular neurobiology of dementing illnesses such as  Alzheimer's disease (AD) and vascular dementia (VD). It's research strategy is focused on the  use of a broad class of drugs modulated by specific genetic variants used or, developped for  the treatment and prevention of neurodegenerative diseases such as AD.   There is an estimated 6 million persons suffering from Alzheimer's disease in North America ( > 36 million worldwide) and twice as many who are "at risk" of developing the disease in the  next 15 years. ADGEN's research team believes that its patented technology and research  approaches represent major advancements in the fight against dementias. It is estimated that  $180 billion dollars are spent every year on direct and indirect health care cost and lost working  days in North America because of Alzheimer's disease. Our pioneering work on the role of  genetic risk factors in disease etiology and therapy has allowed us to identify several genetic  variants that affect either, the age of onset, the rate of progression or the quality of the drug  response to memory enhancer medications. We are also examining closely the interplay  between traumatic brain injury, genetics and the enhanced risk of developping AD. The most  common genetic defect identified so far in the common form of AD involves a critical transporter  of brain cholesterol called apolipoprotein E (apoE) and a neurotransmitter degrading enzyme  called butyrylcholinesterase (BuChE). Using unique genetic signatures, we have characterized  the biological functions of key modulators of lipid physiology in the brain and screened a large  number of chemical entities capable of restoring impaired lipid homeostasis in the brain of  affected AD subjects. This pioneering work led to the successful identification of several  potential pharmacological targets, including a few potent apoE inducers and inhibitors of the  isoprenoid cascade in neurons. In recent year, we choosed to focus on a particular compound which is commonly used in asian  countries to lower blood cholesterol in humans. This led to the development of an extensive  pre-clinical research program in brain rodent and human cell cultures, mice and rat models, and more importantly, to a small proof-of-principle clinical trial in humans suffering from mild-to-  moderate AD. Final results clearly indicate that it is possible to modify the brain's lipid chemistry  and to enhance lipid mobilisation, to slow down disease progression and to reduce the burden  of toxic brain byproducts such as phospho-Tau, a protein commonly associated with AD  pathology. We are now actively pursuing this avenue of research in the context of prevention  using healthy controls with a parental history of AD. The first trial is examining the dose-  response relationship between drug levels and apoE alteration in the human brain. The second  trial to be launched in early 2017 consists of a double-blind, placebo-controlled clinical trial  design to slow down the disease progression and, to postpone the onset of the disease by  several years using biomarker driven outcome analyses.       Although there are a few medications designed to improve memory deficits in AD subjects,  none of these treatments halt or slow down the progression, or delay onset of the disease in a  significant manner. At best, the clinical benefits last 6 to 18 months, and only in a modest  subset of patients. Furthermore, recent attempts by small and large pharmaceutical  corporations to interfere with one of Alzheimer’s pathological hallmark called amyloid by means  of vaccines (Elan, Wyett-Ayerst), inhibitors of synthesis (Astrazeneca, SKB, GSK and Ely Lilly)  and disaggregating agents (Parke-Davis, Neurochem) have failed so far to meet FDA  requirements.   
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© J. Poirier 2017
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