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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. 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. The most common genetic defect  identified so far involves a critical transporter of brain  cholesterol called apolipoprotein E (apoE), as well as many of  its accessory proteins called apoJ, ABCA1 and ABCA7,  BuChE, FDPS, SREBF2, GGDPS and so the called HMGCR.  Using this unique genetic information, we have characterized  the biological functions of these key cholesterol transporter &  modulators in the brain and screened a large number of  chemical entities capable of restoring apoE activity in the brain  of affected AD subjects. This pioneering work led to the  successful identification of several potent apoE inducer agents  which are now in pre-clinical development.  
Research Experience and Opportunities
Research Tools Team Publications  Services and Expertises Team Tools Media Facts Patent Portfolio Team Publication List of key publications describing some of the core discoveries done in the ADGEN unit. Patent Portfolio List of key patents  covering ADGEN research team’s discoveries over the course of the past 20 years.
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