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  1. Mer
    1,357 Posts.
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    Simon - a nice summary, many thanks.

    I haven't placed as much weight on the mice results as the trial extension + HD cognition. A lot of drugs start out by doing well in rodents, but it doesn't always transfer well to people.

    As you've noted, the improvements in wild type mice show that plaque reduction isn't the only process in play here and neural growth might well account for at least some of the cognitive gains. Maybe this is what happened with the HD trial.

    As amyloid measurement is listed as an endpoint, it could take the gloss off patient improvement if it can't be shown to reduce. A patient could show improvement on account of neural growth, yet also show no plaque reduction. This trial should provide information on what mechanism PBT2 is using for patient benefit, but without an amyloid reduction the AD is being offset(against increased number of neurons for instance) rather than treated (reduced plaque load).

    I'm quietly confident of some patient improvement and hopeful that the amyloid results will correlate.

    Cheers - a hopeful pessimist

    dyor
 
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