Interviewer: Professor Hardy, thanks very much for making your time available.
It's very much appreciated since I understand you had a tight grant timeline.
Obviously developing treatments in dementia, Alzheimer's dementia, among others,
is a really great opportunity for pharmaceutical companies if they can do it.
If I understand you correctly,
is it that you have views at the moment
that one potential way to go is to concentrate on the membrane of the cell,
nerve cell, is that correct?
Prof. Hardy: Yes, that is right.
I think that amyloid build ups starts in neuronal membranes,
and that is the site of the initial problem.
If we could just start to help the brain, the particularly microglia,
but other cells to clean up the damaged membranes,
that would be a good target.
Yes. That's what I think.
Interviewer: So, let me ask here, between cleaning up,
the term that you use,
and prevention in the first place,
do you have any views on that?
Prof. Hardy: It's probably different in different cases.
In the cases of the autosomal dominant,
the rare forms of disease,
where mutations are actually in the amyloid protein or in
the proteins which digest the APP molecule to give the amyloid protein,
I think that a direct attack on the buildup of amyloid is absolutely the way forward.
In typical late onset disease which is of course a bit more difficult,