Figure 4. Modelling in animals and what has been achieved so far.

Depending on how much weight we put on the different aspects of AD modelling (symbolized by the ‘M’) in animals the balance of ‘achievement’ will vary. The distribution is not meant to be taken at face value, but thought to provide an idea of which aspects of the human disease need further development. Protein aggregation has been very faithfully modelled in animals, as have aspects of behavioural impairment. Support has been provided for all hypotheses proposed for AD and FTD. Some insight has been achieved into the molecular mechanisms of how soluble tau and the different assembly states of Aβ cause and initiate cellular demise, but a real understanding is still lacking. The more we move to the right, the less has been authentically modelled. There are indeed aspects which, for obvious reasons, cannot be modelled in animals at all, such as the language variants of FTD.