© J. Poirier 2022
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.     
Welcome A Foreword from the ADGEN Research Team
Laboratory Publications
Research Findings  
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