Appeal No. 1997-3122
Application No. 08/082,848
9
Appellants, on the other hand, cite Nagasawa as evidence in support of their
argument that “[t]he pattern of blood vessel occlusion in [ ] stroke models causes any
treatment to be less effective in the striatum than in the cerebral cortex.” Brief, page 8.
Indeed, Sharkey addresses this very effect: “The finding that brain damage is reduced in
cortex but not striatum has been attributed to differences in vascular supply to these brain
areas, and is also typical of the actions of neuroprotective drugs tested in MCA occlusion
models” (page 337, citations omitted). Inasmuch as blood vessel occlusion “is not the
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cause of either Parkinson’s disease or Huntington’s disease,” appellants argue that “[a]
drug’s lack of effectiveness in the striatum in a stroke model provides no reason to infer
that the same drug will not be able to access the striatum in patients who have other
neurological diseases.” Brief, page 8. We would add that we see no reason to infer that a
drug effective in the cortex will not be effective in the striatum; as acknowledged by the
examiner, “the type of damage being treated in the claims (glutamate-mediated
neurotoxicity mediated by NMDA receptors) is the same no matter how caused.”
Examiner’s Answer, page 10.
9Nagasawa & Kogure (Nagasawa), “Correlation Between Cerebral Blood Flow
and Histologic Changes in a New Rat Model of Middle Cerebral Artery Occlusion,” Stroke,
Vol. 20, No. 8, pp. 1037-1043, August 1989.
10 See Beal et al., “Degenerative Diseases of the Nervous System,” in Harrison’s
th
Principles of Internal Medicine, p. 2060, 12 ed., 1991.
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