Appeal No. 1997-2182
Application 08/137,443
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 to5
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)
Simply stated, the examiner has failed to present
objective evidence sufficient to cast doubt on the objective
truthfulness of appellants' assertions made in their
specification and on which they rely for enablement. It is
only after the examiner presents evidence which establishes
that one of ordinary skill in the art would reasonably doubt
the assertions made by appellants in their specification in
support of the enablement requirement of the statute that
1,2,3,4 -tetrahydro-9-aminoacridine, also known as THA.5
13
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