Appeal No. 1997-2167
Application 08/137,444
acknowledge the therapeutic effect of AChE inhibitors for
treating Alzheimer's disease. The examiner has also cited
Sarter et al. as evidence that there was a recognition in the
art at the time appellants made their invention that the high
number of failures in clinical trials for drugs ("recognition
enhancers") screened and then tested on an animal model was
directly correlated to the lack of sufficient attention to the
specific psychological mechanisms underlying behavioral
enhancement. Nevertheless, Sarter et al. do recognize at page
154 that, "[a]rguably the strongest case for positive effects
can be made for the AChE inhibitors," and Sarter et al. also
observe at page 149 that:
AChE inhibitors and muscarinic agonists can reverse
behavioral deficits caused by lesions to the cholinergic
basal forebrain nuclei or drug induced ACh depletion in a
wide variety of learning and memory tasks. (citation
omitted)
Further, both Nordberg et al. and Liston et al. recognize the
mechanism by which Tacrine functions is believed to be due to4
AChE inhibition. Indeed, Liston et al. comment that they:
conclude that the inhibition of brain AChE by THA is
sufficient to explain its therapeutic action in
Alzheimer's disease. (emphasis ours)
1,2,3,4 -tetrahydro-9-aminoacridine, also known as THA.4
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