Appeal No. 2006-0299 Page 2
Application No. 09/964,412
Specification, pages 1-2. “AD neurodegeneration is characterized by prominent
atrophy of corticolimbic structures with neuronal loss, neurofibrillary tangle
formation, aberrant proliferation of neurites, senile plaques, and βA4-amyloid
deposition in the brain.” Id., page 2.
AD7c-NTP cDNA was isolated from a cDNA library prepared from the
temporal lobe of an individual with end-stage Alzheimer’s disease. Specification,
page 33. According to appellants, the 1442-nucleotide AD7c-NTP cDNA “is an
Alu sequence-containing gene” and “encodes a ~41 kD membrane spanning
protein” (id., page 17). AD7c-NTP is expressed in normal brain tissue, but
“[q]uantitation of data obtained from 17 AD and 11 age-matched control brains
demonstrated significantly higher levels of AD7c-NTP gene expression in AD. In
situ hybridization and immunostaining studies localized AD7c-NTP gene
expression in neurons, and confirmed the over-expression associated with AD
neurodegeneration . . . [These] results suggest that . . . abnormal expression of
AD7c-NTP is a phenotype associated with Alzheimer’s disease.” Id., page 18.
In addition, various neuronal cell lines were stably transfected with AD7c-
NTP cDNA and examined for growth properties, morphology, and expression of
AD7c-NTP. Specification, pages 45 and 46. “Over-expression of AD7c-NTP . . .
resulted in significantly lower densities of viable cells in the cultures, despite
normal or elevated levels of DNA synthesis” (id., page 46). The “[r]educed cell
density in the cultures was caused by increased cell death” (id.), as shown by the
invariable presence of “numerous round, refractile floating [dead] cells” (id.).
According to appellants, “[t]he attendant increase in nuclear p53 expression in
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