© 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
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