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© J. Poirier 2021
Under the leadership of Dr. Judes Poirier, C.Q., ADGEN is a 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 several classes of drugs in 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 ( > 40 million worldwide) and twice as many who are "at risk" of developing the disease in the next 15 years. One in three seniors will suffer from AD. ADGEN's research team believes that its  patented technologies and research approaches represent major advancements in the fight  against dementias. It is estimated that $1100 US billion dollars are spent every year on direct and indirect health care cost and lost working days worldwide. Our pioneering work on the role of  genetic risk factors and biomarkers in the disease’s etiology and therapy has allowed us to identify several genetic variants and proteins that affect either, the age of onset, the rate of progression or the quality of the drug response to memory enhancer medications. The most common genetic  defect identified so far involves critical transporters of brain cholesterol called apolipoprotein E  (apoE),  J (apoJ) and more recently, cerebral apolipoprotein B (apoB). Using unique genetic and  protéomic 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 modulators of the isoprenoids cascade. In recent years, we have focused on a particular sets of chemical entities which have been used in the past to treat conditions such as high blood cholesterol or osteoprorosis 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 small proof-of-principle clinical trials in  humans suffering from mild-to-moderate AD and in cognitively unaffected subjects. 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. A few pharmaceutical  corporations have expressed interested in the lipid transporter-based therapy field by launching  new, but small, initiatives to tackle this emerging field of research in AD. 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 (~ 30%). Furthermore, recent attempts by small and large pharmaceutical corporations to interfere with one of Alzheimer’s pathological hallmark called amyloid by means of vaccines (Pfizer, J&J, Eli Lilly, Wyett-Ayerst, Novartis … ), inhibitors of synthesis (Astrazeneca, SKB, GSK, Eisai and Ely  Lilly) and disaggregating agents (Parke-Davis, Neurochem) have failed so far to meet FDA  requirements for approval.     
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