© J. Poirier 2025-2026
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. Our
pioneering work on the role of genetic risk factors and biomakers
in disease etiology and therapy has allowed us to identify several
genetic variants and many cerebrospinal fluid (CSF) biomarkers
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 and B , as well as many of their companion proteins
called ABCA1, ABCG1 and ABCA7, BuChE, CNTN5, FDPS,
GGDPS and the so-called HMGCR, a regulator of cholesterol
synthesis.
Using this unique genetic and proteomic 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 modulating synaptic
plasticity and restoring brain activity of affected AD subjects. This
pioneering work led to the successful identification of several
potent inducer agents which have been tested in pre-clinical
research, one of which in phase 2 trials. Inflammation and
cardiovascular biomarkers are also of prime interest in our
research program, especially for their role in the pre-
symptomatic phase of the disease in subjects who are at-risk of
developping the disease because of a parental history of
Alzheimer’s disease.
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. Our
pioneering work on the role of genetic risk factors and biomakers
in disease etiology and therapy has allowed us to identify several
genetic variants and many cerebrospinal fluid (CSF) biomarkers
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 and B , as well as many of their companion proteins
called ABCA1, ABCG1 and ABCA7, BuChE, CNTN5, FDPS,
GGDPS and the so-called HMGCR, a regulator of cholesterol
synthesis.
Using this unique genetic and proteomic 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 modulating synaptic
plasticity and restoring brain activity of affected AD subjects. This
pioneering work led to the successful identification of several
potent inducer agents which have been tested in pre-clinical
research, one of which in phase 2 trials. Inflammation and
cardiovascular biomarkers are also of prime interest in our
research program, especially for their role in the pre-
symptomatic phase of the disease in subjects who are at-risk of
developping the disease because of a parental history of
Alzheimer’s disease.
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 30 years.
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 30 years.
