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damage has been inflicted. Disease-modifying therapies are most likely

to influence progression to disease and/or delay onset of symptoms.

Proper assessment of the effects of a therapy will require clinical trial

designs that make the appropriate measurements. It will be important

to assess plaque load and/or h-peptide level in patients treated with

aggregation inhibitors or other modes of reducing either brain hpeptide content or its effects in addition to the classical cognitive end

points. Whatever the outcome of the trials, in interpreting the results

for the development of new generations of therapeutics it is important

to determine whether the therapy accomplished what it was designed to

do—reduce amyloid peptide deposition. If h peptide is eliminated but

no therapeutic benefit is observed, we should conclude that the h

peptide is not the major player—at least in the patient population selected for study. The answer will be important in justifying future

pharmaceutical investment as well as in guiding future research for

effective therapies against AD.


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