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0:00
Well, it's my honor to present
some of the insights we've
developed in Alzheimer's
disease over the last 40 years.
In particular, I'm
going to talk about
brain aging at a crossroads.
Where do we go from three
decades of failed therapeutics?
0:21
The work I'm going to present is
a collaboration
among many people.
I've listed many of them here,
both at the University
of Texas San Antonio,
where I now work.
Case Western Reserve University,
where I used to work,
as well as collaborator is
spread throughout the world,
and I'll mention some of them.
0:40
When you talk about
Alzheimer's disease,
one of the key issues
is where did it start.
I'll come back to
this later because
that description by
Alois Alzheimer's in
1906 still sets the
framework for now,
whether it's molecular biology,
genetics, protein
chemistry, radiomics.
Most people relate it
Alzheimer's disease is
a dementing loss of higher
cognitive function associated
with senile plaques of
amyloid and
neurofibrillary tangles
within neurons at risk of death.
Those three things
together form the basis
of Alzheimer's disease and
the basis of therapeutics.
1:27
But knowing that
Alzheimer's disease
is plaques and tangles,
and over 100 years of studies,
nearly 120 years of intensive
research, well funded,
how has that played out
in having a therapeutic?
Well, there's been
hundreds of thousands
of papers published in it.
There's been increased
funding from foundations.
But yet the only effective
therapeutics that are
approved have at best
addressed symptoms
and only work for a short time,
and the recently approved
monoclonal antibodies
don't even address
those symptoms.
They may slow the
course of the disease.
None of them reverse
the progression of
Alzheimer's disease.
With that in mind,
there's been a
99.6% failure of new
drug development
in Alzheimer's disease.
What I want to cover in the
rest of this talk is has
the focus been so long on
removing plaques and tangles,
in other words, removing
the changes of aging
that occur in the brain.
Now with the advanced monoclonal
antibodies that are effective in
removing amyloid for the brain,
and with marginal
clinical benefit at best.
Haven't we tested that the
answer is not so simple?
How do we go beyond this?
What we've done over the past
30-plus years is look at
