© J. Poirier 2025-2026
Under the leadership of Dr. Judes Poirier, K.Q, MD (Hon), 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, biomarkers and genetic variants 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
( > 50 million worldwide) and twice as many who are "at risk" of developing the disease in the next
25 years. One in three seniors will suffer from AD. ADGEN's research team believes that its
research approaches represent major advancements in the fight against dementias. It is estimated
that more than $1,500 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 drugs and disease progression modulators such as the new anti-
amyloid agents such as lecanemab and donanemab. 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 proteomic
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 and apoB
inducers as well as new 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 rodents 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 at-risk but 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 synaptic and amyloid/tau
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 significantly 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, Eisai, Biogen) have led generally to poor results or
modest reduction (~30%) in cognitiive decline, and only in subjects selected on the basis of
significant brain amyloid load, excluding a significant number of patients, particularly african
americans and latinos. Inhibitors of amyloid synthesis (Astrazeneca, SKB, GSK, Eisai and Ely
Lilly) and disaggregating agents (Parke-Davis, Neurochem) have all failed so far to meet FDA
requirements for approval.
disease (AD) and vascular dementia (VD). It's research strategy is focused on the use of several
classes of drugs, biomarkers and genetic variants 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
( > 50 million worldwide) and twice as many who are "at risk" of developing the disease in the next
25 years. One in three seniors will suffer from AD. ADGEN's research team believes that its
research approaches represent major advancements in the fight against dementias. It is estimated
that more than $1,500 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 drugs and disease progression modulators such as the new anti-
amyloid agents such as lecanemab and donanemab. 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 proteomic
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 and apoB
inducers as well as new 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 rodents 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 at-risk but 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 synaptic and amyloid/tau
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 significantly 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, Eisai, Biogen) have led generally to poor results or
modest reduction (~30%) in cognitiive decline, and only in subjects selected on the basis of
significant brain amyloid load, excluding a significant number of patients, particularly african
americans and latinos. Inhibitors of amyloid synthesis (Astrazeneca, SKB, GSK, Eisai and Ely
Lilly) and disaggregating agents (Parke-Davis, Neurochem) have all failed so far to meet FDA
requirements for approval.
Welcome
A Foreword from the ADGEN Research Team
Laboratory Publications
Databases
Research Findings
