© J. Poirier 2022
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
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,
FDPS,
GGDPS
and
the
so-called
HMGCR.
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
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