CONCLUSIONS
What will the next generation of transgenic
models of AD bring, and how can they be developed
to help develop therapeutics and preventatives
for sporadic AD? A new era will be
ushered in as other types of animal models are
produced. For example, there may be advantages
to moving away from mice and rats and
genetically modifying other smaller animal species,
particularly those in which the endogenous
Ab sequence is identical to humans and those in
which processing of tau is more closely aligned
to humans. In addition, we need to find ways
to model sporadic AD, rather than familial
AD. This means that the animals will need to
develop pathology because they age, rather
than because their genes program them to do
so. Once such an animal is produced we will
be able to study which aspects of the aging process
drive the pathology in the first place, and
then target them for prevention. We have
already proposed using alternative models of
neuronal loss to supplement AD pathology
models, and think that this is also a good
approach. Making such models will be challenging
and will require a great deal of investment,
both time and financial, and not all
approaches will work. However, we need to
improve on the current batch of AD transgenics
and look to future so that we will be able to treat
and prevent this insidious disease.