Appeal No. 1997-3122
Application No. 08/082,848
Sharkey demonstrates that “FK506 is a powerful neuroprotective agent in an in vivo
model of focal cerebral ischaemia of equivalent efficacy to the non-competitive NMDA
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receptor antagonist, MK801,” a known neuroprotective agent. Page 337, left-hand
column. The examiner acknowledges that “[c]ortical damage was inhibited,” but argues
that “striatal damage was unaltered by any dose of FK-506 . . . [i]n addition, the ligands
cyclosporin and rapamycin failed to protect.” Thus, according to the examiner, “primary
cerebral cortical neuronal cultures . . . are not predictive of the in vivo situation for at least
stroke in parts of the brain other than the cortex,” nor is the specification enabling for drugs
other than FK-506. Moreover, the examiner argues that Sharkey’s results “provide reason
to doubt that the claimed method would be suitable for treating [Parkinson’s disease and
Alzheimer’s disease] and that the in vitro model of the specification would not be
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predictive,” because striatal tissue is affected in both diseases. Examiner’s Answer,
page 9.
7According to Sharkey, “[a]nimal models of focal cerebral ischaemia based on
middle cerebral artery (MCA) occlusion reproduce the pattern of ischaemic brain damage
observed in many human stroke patients” and “[d]amage extends throughout the vascular
territory of the MCA: that is, within the striatum and cortex.”
8As evidence of striatal involvement in Parkinson’s disease and Alzheimer’s
disease, the examiner cites Ulas et al., “Selective Increase of NMDA-Sensitive Glutamate
Binding in the Striatum of Parkinson’s Disease, Alzheimer’s Disease, and Mixed
Parkinson’s Disease/Alzheimer’s Disease Patients: An Autoradiographic Study,” The
Journal of Neuroscience, Vol. 14, No. 11, pp. 6317-6324 (November 1994).
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