Wurtman et al.v.Hageman et al.

Patent Trial and Appeal Board

Mar 29, 2019

11920914 (P.T.A.B. Mar. 29, 2019)

BoxInterferences@uspto.gov Filed: March 29, 2019
Tel: 571-272-9797

UNITED STATES PATENT AND TRADEMARK OFFICE
_______________

BEFORE THE PATENT TRIAL AND APPEAL BOARD
_______________

N.V. Nutricia
(Inventors: Robert Johan Joseph Hageman,
Patrick Joseph Gerardus Hendrikus Kamphuis, and Ladislaus Maria Broersen)

Junior Party
(Patent 8,445,458),

v.
Massachusetts Institute of Technology
(Inventors: Richard J. Wurtman and Ingrid Richardson)

Senior Party
(Patent Application 11/920,914).

Patent Interference No. 106,096 (DK)
(Technology Center 1600)

JUDGMENT
37 C.F.R. § 41.127(a)

Before SALLY GARDNER LANE, JAMES T. MOORE, and DEBORAH KATZ,
Administrative Patent Judges.

KATZ, Administrative Patent Judge.

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2

Junior Party N.V. Nutricia (“Nutricia”) was accorded benefit of the filing
date, 20 June 2008, of its international application PCT/NL2008/050408. (See
Declaration, Paper 1, 5:12.) Senior Party Massachusetts Institute of Technology
(“MIT”) was accorded benefit of the filing date, 23 May 2006, of its international
application PCT/US06/19766. (See Declaration, Paper 1, 5:13.) Nutricia filed a
priority statement, but did not assert a date of conception or reduction to practice
earlier than the filing date, 20 June 2008, of its international application,
PCT/NL2008/050408, which was accorded to it upon declaration. (See N.V.
Nutricia Priority Statement, Paper 42; see Declaration, Paper 1, 5:12.) MIT was
accorded benefit of an earlier filing date, 23 May 2006, upon declaration. (See
Declaration, Paper 1, 5:11–13.) Therefore, Nutricia cannot assert an earlier date of
invention. See 37 C.F.R. § 41.204(a)(1) (“A party may not submit evidence of its
priority in addition to its accorded benefit unless it files a statement setting forth all
bases on which the party intends to establish its entitlement to judgment on
priority.”). Accordingly, Nutricia involved claims are unpatentable under 35
U.S.C. § 102(g).1
We denied Nutricia Motion 1 arguing that claims 2 and 9 of Nutricia’s
involved patent 8,445,458 do not correspond to Count 1. (See Decision on
Motions, Paper 80.)
It is ORDERED that Nutricia patent 8,445,458, claims 1–10 be
CANCELED;

1 Patent interferences continue under the relevant statutes in effect on March 2013.
See Pub. L. 112-29, § 3(n), 125 Stat. 284, 293 (2011).
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3

It is also ORDERED that a copy of this judgment shall be entered into the
administrative record of patent 8,445,458, application 11/920,914;
It is further ORDERED that the parties are directed to 35 U.S.C. § 135(c)
and to 37 C.F.R. § 41.205 regarding the filing of settlement agreements; and it is
further ORDERED that a party seeking judicial review timely serve notice on the
Director of the United States Patent and Trademark Office; 37 C.F.R. §§ 90.1 and
104.2. See also 37 C.F.R. § 41.8(b). Attention is directed to Biogen Idec MA, Inc.,
v. Japanese Foundation for Cancer Research, 785 F.3d 648, 654–57 (Fed. Cir.
2015) (determining that pre-AIA § 146 review was eliminated for interference
proceedings declared after September 15, 2012).

cc (via e-mail):
Attorney for Junior Party Nutricia
David R. Fairbairn
Alan M. Koenck
KINNEY & LANGE, P.A.
drfairbairn@kinney.com
amkoenck@kinney.com

Attorney for Senior Party MIT

Mark Cohen
Craig L. Puckett
PEARL COHEN ZEDEK LATZER BARATZ LLP
mcohen@pearlcohen.com
cpuckett@pearlcohen.com

BoxInterferences@uspto.gov Filed: March 29, 2019
Tel: 571-272-9797

UNITED STATES PATENT AND TRADEMARK OFFICE
_______________

BEFORE THE PATENT TRIAL AND APPEAL BOARD
_______________

N.V. Nutricia
(Inventors: Robert Johan Joseph Hageman,
Patrick Joseph Gerardus Hendrikus Kamphuis, and Ladislaus Maria Broersen)

Junior Party
(Patent 8,445,458),

v.
Massachusetts Institute of Technology
(Inventors: Richard J. Wurtman and Ingrid Richardson)

Senior Party
(Patent Application 11/920,914).

Patent Interference No. 106,096 (DK)
(Technology Center 1600)

Decision on Motions
37 C.F.R. § 41.125(a)
Before SALLY GARDNER LANE, JAMES T. MOORE, and DEBORAH KATZ,
Administrative Patent Judges.

KATZ, Administrative Patent Judge.
Introduction
N.V. Nutricia (“Nutricia”) is involved in this interference as the junior party
based on its patent 8,445,458 (“the ’458 patent”). Claims 1–10, all of the claims of
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the ’458 patent, were designated as corresponding to Count 1. (See Declaration,
Paper 1, 5:1–10.) Nutricia was accorded benefit of the filing date, 20 June 2008, of
its international application PCT/NL2008/050408. (See Declaration, Paper 1,
5:12.)
Massachusetts Institute of Technology (“MIT”) is involved based on its
application 11/920,914. All of the claims of the ’914 application were designated
as corresponding to Count 1. (See Declaration, Paper 1, 5:1–10.) MIT was
accorded benefit of the filing date, 23 May 2006, of its international application
PCT/US06/19766. (See Declaration, Paper 1, 5:13.)
Both parties claim methods comprising administering a composition to a
person to treat conditions related to dementia. (See ’458 patent, Ex. 2002, abstract;
see ’914 appl., Ex. 2001, abstract.) The compositions recited in both parties’
claims include omega 3 fatty acid, uridine or a derivative thereof, and a methyl
donor, such as choline. Count 1 describes the interfering subject matter and was
determined to be the same as MIT claim 49.
The parties filed motions during this preliminary, non-priority phase of the
interference. Senior Party MIT filed three motions: Motion 1 arguing that it should
be accorded the benefit of a provisional application (Paper 44); Motion 2 arguing
that Nutricia’s involved claims are unpatentable under 35 U.S.C. § 112, first
paragraph (Paper 45); and Motion 3 arguing that Nutricia’s involved claims are
unpatentable under 35 U.S.C. § 102(b) (Paper 46).
MIT’s motions are moot because Nutricia did not assert a priority date
earlier than MIT’s accorded benefit date. Specifically, Nutricia filed a priority
statement, but did not assert a date of conception or reduction to practice earlier
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than the filing date, 20 June 2008, of its international application,
PCT/NL2008/050408, which was accorded to it upon declaration. (See N.V.
Nutricia Priority Statement, Paper 42; see Declaration, Paper 1, 5:12.) MIT was
accorded benefit of an earlier filing date, 23 May 2006, upon declaration. (See
Declaration, Paper 1, 5:11–13.) Nutricia cannot assert a date of invention earlier
than 20 June 2008 in a priority phase of the interference. See 37 C.F.R.
§ 41.204(a)(1) (“A party may not submit evidence of its priority in addition to its
accorded benefit unless it files a statement setting forth all bases on which the
party intends to establish its entitlement to judgment on priority.”). Accordingly,
Nutricia cannot win on priority and its claims involved in the interference will be
canceled under 35 U.S.C. § 135(a).1 The motions filed by MIT, asserting an even
earlier priority date and that Nutricia’s claims are unpatentable under different
statutes are, therefore, moot and we DISMISS them.2
Junior Party Nutricia filed Motion 1, arguing that claims 2 and 9 of its
involved ’458 patent do not correspond to Count 1. (Paper 26.) Claims not
corresponding to Count 1 are not involved in the interference and will not be
canceled under 35 U.S.C. § 135(a). Therefore, we take up Nutricia Motion 1, to

1 Patent interferences continue under the relevant statutes in effect on March 2013.
See Pub. L. 112-29, § 3(n), 125 Stat. 284, 293 (2011).
2 MIT requested oral argument, specifically on the issues raised in its Motions 2
and 3. (See Paper 79.) Because these motions are moot, we exercise our discretion
and decline to hold an oral argument. See 37 C.F.R. § 41.124(c)(“If a request for
oral argument is granted . . . .”).
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determine which of its claims will be canceled when judgment is entered. For the
reasons that follow, we DENY Nutricia Motion 1.
Nutricia Motion 1
Nutricia argues that claims 2 and 9 of its involved ’458 patent should not be
designated as corresponding to Count 1 and, thus, are not involved in the
interference. (See Nutricia Motion 1, Paper 26, 1:7–10.) “A claim corresponds to
a count if the subject matter of the count, treated as prior art to the claim, would
have anticipated or rendered obvious the subject matter of the claim.” 37 C.F.R.
§ 41.207(b)(2). Thus, it is Nutricia’s burden to persuade us that Count 1 would not
anticipate or render obvious claim 2 or claim 9 of its involved ’458 patent. See
37 C.F.R. § 41.208(b)(“To be sufficient, a motion must provide a showing,
supported with appropriate evidence, such that, if unrebutted, it would justify the
relief sought. The burden of proof is on the movant.”); see also 37 C.F.R.
§ 41.121(b).
Count 1 is claim 49 of MIT’s involved ’914 application and recites:
A method of increasing an amount of a synaptic membrane of a neural
cell or brain cell of a subject comprising
administering to said subject in need of such treatment a
therapeutically effective amount of a composition having:
(a) an omega-3 fatty acid, an omega-6 fatty acid, or a combination
thereof;
(b) uridine, an acyl derivative thereof, a uridine phosphate or a CDP22
choline; and
(c) a choline salt,
wherein uridine, an acyl derivative thereof, a uridine phosphate or
CDP-choline is dosed to provide a range of 10 to 500 mg of uridine per day
and choline is dosed in a range of 100 mg to 10 g per day.

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(Declaration, Paper 1, 4:12–26.)
Claim 2
We consider Nutricia’s arguments regarding claim 2 first.
Nutricia’s claim 1 recites:
A method for the prevention or delay of the onset of dementia in a
person having characteristics of a prodromal dementia patient comprising
administering to the person a composition comprising:
(a) one or more ω-3 fatty acids selected from DHA, DPA and EPA,
(b) a uridine selected from the group of uridine, deoxyuridine, uridine
phosphates, uracil and acylated uridine derivatives, and
(c) a methyl donor.

(N.V. Nutricia Clean Copy of Involved Claims, Paper 6, 3:1–9.)
Nutricia’s claim 2 recites:
The method according to claim 1, wherein the characteristics
comprise two or more of:
a level of more than 350 ng Total-tau per liter cerebrospinal fluid
(CSF);
a weight ratio of abeta-42/Phospho-tau-181 of less than 6.5 in CSF;
presence of medial temporal lobe (MTL) atrophy, existing of volume
loss of hippocampus, entorhinal cortex, or amygdala evidenced
on Magnetic Resonance Imaging (MRI);
presence of fronto-temporal lobe (FTL) atrophy evidenced on MRI
with qualitative ratings or quantitative volumetry;
a level of more than 25 pg F2-iso-prostane (F2-IsoP, isoprostane 8,12-
iso iPF2alpha-VI) per mL CSF; reduced glucose metabolism in
bilateral temporal parietal areas of the brain, as is detectable by
Positron Emission Tomography (PET);
reduced glucose metabolism in the posterior cingulate cortex, as is
detectable by PET;
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impaired blood flow in the brain as measurable by applying Single-
Photon Emission Computed Tomography (SPECT), for
example by applying the radioisotope 99mTc-HMPAO);
impaired glucose metabolism in the brain as measurable by applying
SPECT;
abnormalities in the histology of the medial or inferior temporal lobes
as can be determined by MRI or in the rate of glucose
utilisation;
abnormalities in histology or glucose utilization in the temporal
parietal cortex or posterior cingulate cortex.

(N.V. Nutricia Clean Copy of Involved Claims, Paper 6, 3:11–4:10.)
Nutricia argues that Count 1 does not anticipate claim 2. (See Nurticia
Motion 1, Paper 26, 7:19–22.) Specifically, Nutricia argues that Count 1 does not
teach any characteristics of “prodromal dementia” or the diagnostic criteria by
which prodromal dementia patients are determined, which are the limitations of
claim 2.
We agree with Nutricia that the language used in Count 1 and claim 2 is
different. Count 1 refers to a “subject in need of [such] treatment,” wherein the
treatment increases an amount of synaptic membrane of a neural cell or brain cell.
(Declaration, Paper 1, 4:12–26.) In contrast, Nutricia’s claim 2 refers to
preventing or delaying the onset of dementia in “a person having the characteristics
of a prodromal dementia patient” and recites a choice of two from a long list of
specific criteria. (N.V. Nutricia Clean Copy of Involved Claims, Paper 6, 3:11–
4:10.) “Anticipation requires a showing that each limitation of a claim is found in
a single reference, either expressly or inherently.”Atofina v. Great Lakes Chem.
Corp., 441 F.3d 991, 999 (Fed. Cir. 2006). Thus, regardless of the specific
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language used in claim 2, Nutricia must persuade us that preventing or delaying the
onset of dementia in a person have the specific characteristics of prodromal
dementia recited in claim 2 is not the same as increasing the amount of a synaptic
membrane in a neural or brain cell in a subject in need of such treatment as recited
in Count 1.
Nutricia’s explains that “[p]rodromal dementia patients do not suffer from a
senile dementia, but have an increased likelihood to develop senile dementia.”
(Nutricia Motion 1, Paper 26, 4:15–16; see also ’458 patent, Ex. 2002, 3:55–57
(“[a] ‘prodromal dementia patient’ is a person who does not suffer from a senile
dementia as defined above, but has an increased likelihood to develop senile
dementia.”).) We understand “prodromal dementia” to be a condition or stage
before dementia is diagnosed.
Nutricia argues that Count 1 and MIT’s application refer to treating patients
with actual dementia or deterioration in memory, not prodromal dementia. (See
Nutricia Motion 1, Paper 26, 4:24–5:1.) According to Nutricia, “[t]he
distinguishing tests for diagnosing prodromal dementia patients do not coincide
with conventional tests for diagnosing dementia or dementia-like disorders.”
(Nutricia Motion 2, Paper 26, 5:1–4.) In support, Nutricia refers to the
specification of its involved ’458 patent, which states:
The distinguishing tests for diagnosing prodromal patients do not
coincide with conventional tests for diagnosing dementia or dementia-like
disorders, though some of these conventional tests may further support the
diagnosis of a prodromal patient for a neurological disorder or disease. For
example, prodromal [Alzheimer’s disease] patients may score satisfactorily
in a memory test, and will therefore not necessarily be [mild cognitive
impairment] patients, whereas they may score positively in the present
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diagnostic tools for being prodromal. Then the diagnosis “prodromal
dementia patient” is made. Such non-[mild cognitive impairment] group
fulfilling the requirements of the diagnosis of a “prodromal dementia
patient” has not been addressed by Hansson et al. published in
http://neurology.thelancet.com, Feb. 6, 2006. The non-MCI group
demonstrating the same score in the proposed tests was not investigated.

(’458 patent, Ex. 2002, 2:25–39 (emphasis added); see Nutiricia Motion 1,
Paper 26.) Although supporting that the tests for diagnosing dementia and
prodromal dementia do not “coincide,” Nutricia’s specification leaves open the
question of how related diagnosing prodromal dementia is to diagnosing
dementia.3 This portion of Nutricia’s specification states that there is at least some
overlap in the diagnostic tests for prodromal dementia and dementia because it
states that the conventional test for diagnosing dementia “may further support the
diagnosis of a prodromal patient for a neurological disorder or disease.” (’458
patent, Ex. 2002, 2:25–34.) Thus, the specification leaves open the possibility that
prodromal dementia patients exhibit a subset of the characteristics of dementia
patients who have progressed to mild cognitive impairment.
Nurtricia argues that its inventors “found that prodromal patients benefit
from the administration of the composition disclosed in the Nutricia patent because
it decreases the development of more severe problems that are associated with

3 We note that Nutricia does not argue that there is no interference-in-fact between
its claims and MIT’s claims even though Nutricia claim 1, and thus all of
Nutricia’s claims, recite “[a] method for the prevention or delay of the onset of
dementia in a person having the characteristics of prodromal patients . . . ,” and
MIT’s claims all recite a method of administering to a “subject in need of such
treatment . . . .”
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brain malfunction, such as memory and cognition problems, tremor, decrease in
intensity in feelings and sensation, and may decrease or delay the incidence of
dementia.” (Nutricia Motion 1, Paper 26, 7:8–12.) We are not persuaded by this
argument because Nutricia fails to direct us to evidence that the same is not true of
treating patients in need of increasing synaptic membrane. Apparently, both
conditions – the need for increased synaptic membrane and prodromal dementia
defined by the characteristics listed in claim 2 – can be treated by administering a
composition as set forth in the count and claim 2. Nutricia does not direct us to
evidence, such as witness testimony, to show that one of ordinary skill in the art
would have considered a patient having the characteristics of prodromal dementia
to not also have been in need of increased synaptic membrane. We are not
persuaded that one of ordinary skill in the art would not have considered the
patient populations recited in Count 1 and claim 2 to be the same.
Nutricia refers to the prosecution of MIT’s current claims, including MIT
claim 49, which is the count, to support its argument. According to Nutricia, MIT
asserted that “a subject in need of such treatment” is “an individual who is affected
by disease or trauma who has a deficient amount of synaptic membrane of a neural
cell or brain cell and is therefore in need of medical treatment.” (See Nutricia
Motion 1, Paper 26, 5:6–10, quoting Amendment filed 7 April 2011in MIT
’419 appl., Ex. 2005, 13.) Nutricia asserts that the MIT application is focused on
subjects who by illness or injury are in need of medical treatment and subjects
“with specific memory-related diseases or cognitive impairment.” (See Nutricia
Motion 1, Paper 26, 6:5–7.) Nutricia argues that even if the MIT application is
determined to define a general class of patients who need treatment, the specific
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class of prodromal dementia patients “set out [i]n the Nutricia patent would be
patentable over the MIT application.” (Nutricia Motion 1, Paper 26, 6:21–7:7.)
Again, we are not persuaded because this evidence does not persuade us that
prodromal dementia patients are not individuals affected by disease or trauma who
have a deficient amount of synaptic membrane or a neural or brain cell. Nothing
that Nutricia points to in the prosecution history of MIT claim 49 indicates that
“persons in need of such treatment” would not have at least two of the
characteristics provided in Nutricia’s claim 2.
MIT argues4 that
[t]he diagnostic recitations of claim 2 are identical to tests used to diagnose[]
Alzheimer’s disease (AD) patients. The semantic distinction set forth by
Nutricia is a distinction without difference as there is no diagnostic
difference between AD patients and the “prodromal dementia patient” of the
claims. The diagnostic criteria of claim 2 is no different than AD diagnostic
tests, as illustrated by the prior art.

(MIT Opp. 1, Paper 51, 4:5–9.) In support, MIT cites research articles that report
characteristics, such as those recited in Nutricia claim 2, in patients with mild
cognitive impairment, not those with only a risk of developing dementia.
Specifically, MIT cites to Hansson5 (Ex. 1010), arguing that it demonstrates
that incipient Alzheimer’s patients who demonstrate mild cognitive impairment

4 MIT asserts that the count is claim 49 of MIT’s involved application and
claims 1, 2, and 9 of Nutricia’s ’458 patent. (See MIT Opp. 1, Paper 51, 3:12–13.)
Count 1 recites only MIT claim 49. (See Declaration, Paper 1, 4:12–26.) Claims
that correspond to a count are involved in the interference, but do not define the
count. See 37 C.F.R. §§ 41.201 and 41.207(b)(2).
5 Hansson et al., “Association between CSF biomarkers and incipient Alzheimer’s
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can also have levels of factors in the cerebrospinal fluid (“CSF”) within the ranges
recited in claim 2. (See MIT Opp. 1, Paper 51, 4:10–5:6.) Table 2 of Hansson
reports that the CSF of patients with mild cognitive impairment due to Alzheimer’s
disease has a mean “T-tau” level of 816 ng/L and a mean “Aβ42/P-tau181 ratio” of
3.7. (See Hansson, Ex. 1010, 230, Table 2.) These two characteristics meet the
limitations of Nutricia’s claim 2, wherein the characteristics of a prodromal
dementia patient include “a level of more than 350 ng Total-tau per liter
cerebrospinal fluid (CSF) [and] a weight ratio of abeta-42/Phospho-tau-181 of less
than 6.5 in CSF . . . .” (See Nutricia Clean Copy of Claims, Paper 6, at 3:13–14.)
MIT also cites to Patricò6 (Ex. 1011), arguing that it demonstrates that
patients with mild cognitive impairment and Alzheimer’s disease have levels of
CSF factors that would characterize them as prodromal dementia patients by the
criteria of claim 2. (See MIT Opp. 1, Paper 51, 5:7–18.) Patricò teaches that some
patients with mild cognitive impairment and Alzheimer’s disease have
significantly increased levels of 8,12-iso-iPF2α-VI over control subjects, including
more than 25 pg/ml CSF. (See Patricò, Ex. 1011, 974, Figure C.) This increased
level falls within the range recited in Nutricia claim 2 of “a level of more than
25 pg F2-iso-prostane (F2-IsoP, isoprostane 8,12-isoiPF2alpha-VI) per mL
CSF. . . .” (See Nutricia Clean Copy of Claims, Paper 6, 3:20–21.)

disease in patients with mild cognitive impairment: a follow-up study,” 5 THE
LANCET 228–34 (2006).
6 Praticò et al., “Increase in Brain Oxidative Stress in Mild Cognitive Impairment,”
59 ARCH. NEUROL. 972—76 (2002).

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MIT does not cite to testimony to support how one of ordinary skill in the art
would have understood these results. Nevertheless, we are not persuaded that the
results demonstrate that subjects with mild cognitive impairment and Alzheimer’s
disease can have at least some of the limitations recited in Nutricia’s claim 2 as
being characteristics of prodromal dementia. Nutricia argues7 that Hansson and
Patricò show only overlapping diagnostic criteria, not that prodromal dementia
patients are coexistent and identical. (See Nutricia Reply, Paper 76, 3:1–8.) But,
the patient groups need not be identical for Count 1 to anticipate or render obvious
claim 2. Instead, claim 2 is anticipated or rendered obvious if prodromal patients

7 Nutricia refers to arguments it made in Nutricia Opposition 3 in regard to
Hansson and Practicò. (See Nutricia Reply 1, Paper 76, 3:5–6.) The Standing
Order issued with the Declaration in this interference prohibits incorporation by
reference to arguments made in other papers. See Standing Order, Paper 2, ¶ 106.2
(“Incorporation by reference and combined papers are prohibited to reduce the
chance risk of overlooking an argument and to improve the efficiency of decision
making. Incorporation of arguments by reference amounts to a self-help increase in
the length of the brief and a pointless imposition on the Board's time. Each motion,
opposition, and reply must make all arguments accessible to readers, rather than
ask them to play archeologist with the record. [citation omitted]”).) In general,
Nutricia’s arguments against reliance on Hansson and Practicò in its Opposition 3
are that the identification of some overlapping diagnostic criteria does not indicate
that prodromal dementia patients are coextensive or identical with patients
demonstrating mild cognitive impairement or dementia. (See Nutricia Opp. 3,
Paper 70, 5:5–8:19.) This argument is unpersuasive because, as discussed above,
the issue is whether it would have been obvious that prodromal patients are
subjects in need of increasing an amount of synaptic membrane of a neural or brain
cell, as recited in Count 1. We decline to address Nutricia’s specific arguments
because they were not made in Nutricia’s Reply 1.
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are subjects in need of increasing an amount of synaptic membrane of a neural or
brain cell.
The data presented in Hansson and Patricò shows that patients with mild
cognitive impairment can have two or more of the characteristics recited in
claim 2, which are also characteristics of those with mild cognitive dementia.
Thus, we find Hansson and Patricò to be evidence that patients in need of treatment
can be patients who meet the requirements of claim 2. Nutricia’s argument that the
subjects of Count 1 differ from those of claim 2 because only the former need
treatment does not persuade us otherwise. (See Nutricia Motion 1, Paper 26, 5:5–
6:20.)
Nutricia also argues that Claim 2 of its involved ’458 patent is not rendered
obvious by Count 1 in combination with any relevant prior art. (See Nutricia
Motion 1, Paper 26, 8:1–9:14.) Nutricia argues that Claim 2 was rejected as being
obvious over the publication of MIT’s national stage application from which
MIT’s involved application was filed, but ultimately allowed after Nutricia raised
arguments similar to Nurtricia’s aguments discussed above. (See Nutricia
Motion 2, Paper 26, 8:4–25.) According to Nutricia “[a]s shown from this, claim 2
is not rendered obvious over Wurtman, which also forms the basis for the Count.”
(Nutricia Motion 1, Paper 26, 8:24–25.) As explained above, we are not persuaded
by Nutricia’s arguments. Neither the Board nor a party are bound by an ex parte
decision made during prosecution by another party. A motion in an interference is
not an appeal from the examiner's decision, but an independent request to the
Board. See Glaxo Wellcome, Inc. v. Cabilly, 56 USPQ2d 1983, 1984 (BPAI (ITS)
2000).
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The preponderance of the evidence does not persuade us that Nutricia
claim 2 is not anticipated or rendered obvious by Count 1. We are not persuaded
that claim 2 should be designated as not corresponding to Count 1.
Claim 9
Nutricia argues that Count 1 does not anticipate or render obvious Nutricia
Claim 9 and that, therefore, Claim 9 should be designated as not corresponding to
Count 1. (Nutricia Motion 1, Paper 26, 9:15–18:9.) Nutricia Claim 9 recites:
The method according to claim 1, wherein the composition further
comprises one or more B-vitamins.

(N.V. Nutricia Clean Copy of Involved Claims, Paper 6, 5:6–7.)
Nutricia argues that Count 1 does not anticipate Claim 9 because it does not
recite administering a composition that comprises one or more B-vitamins. (See
Nutricia Motion 1, Paper 26, 9:19–10:4.) We agree.
Nutricia argues, further, that Count 1 does not render claim 9 obvious raising
issues similar to those it raised in regard to the correspondence of claim 2. In
general, Nutricia argues that because the prior art did not recognize administering a
composition comprising one or more B-vitamins to a patient having the
characteristics of prodromal dementia to prevent or delay the onset of dementia,
claim 9 would not be obvious over Count 1. (See Nutricia Motion 1, Paper 26,
10:5–12:17.) We are not persuaded by these arguments, because, as discussed
above, we are not persuaded that patients having the characteristics of prodromal
dementia patients, for example as recited in claim 2, are necessarily different from
patients who exhibit mild cognitive dementia or other symptoms of dementia and
are in need of increased synaptic membrane in a neural or brain cell. Thus, prior
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art that teaches using B-vitamins to treat mild cognitive impairment or other
symptoms of dementia could show that including B-vitamins in the composition of
Nutricia claim 1, as recited in Nutricia claim 9, would have been obvious over
Count 1 to those of ordinary skill in the art.
Specifically, we disagree with Nutricia that the teachings in Quadri8
(Ex. 2009) do not show that claim 9 would have been obvious over Count 1
because Quadri does not identify patients having the characteristics of prodromal
dementia. (See Nutricia Motion 1, Paper 26, 10:7–11:7; see also id. at 11:8–12:5.)
Nutricia argues that Quadri “connects the lack of folate with a group of subjects
which already have cognitive impairment.” (Nutricia Motion 1, Paper 26, 10:22–
23.) As discussed above, the evidence cited by MIT shows that subjects described
as having mild cognitive impairment could also fall within the scope of a person
having characteristics of prodromal dementia, as identified in Nutricia claim 2.
Contrary to Nutricia’s argument, the correlation between a lack of folate and
subjects with cognitive impairment reported in Quadri supports the obviousness of
Nutricia claim 9 over Count 1.
Nutricia argues that Quadri questions whether low B-vitamin concentrations
have a role in disease pathology and therefore does not state or imply that
supplementing with B-vitamin would reduce the risk of Alzheimer’s disease or
vascular dementia. (See Nutricia Motion 1, Paper 26, 11:1–7.) Quadri states that

8 Quadri et al., “Homocysteine, folate, and vitamin B-12 in mild cognitive
impairment, Alzheimer’s disease and vascular dementia,” 80 AM. J. CLIN.
NUTRITION 114–22 (2004).
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its reported findings “suggest that relative folate deficiency may precede
[Alzheimer’s disease] and [vascular dementia] onset.” (Quadri, Ex. 2009,
abstract.) Similarly, Quadri states: “The results of the current cross-sectional study
seem to indicate that relative folate deficiency may already be present before the
onset of dementia and, more generally, may represent a risk factor for cognitive
decline in the elderly.” (Quadri, Ex. 2009, 120.) Quadri concludes:
Because associations are not proof of a causal relation, large randomized
controlled clinical trials of the effect of B vitamin supplementation on
reductions in the risk of incident [Alzheimer’s disease] and [vascular
dementia] or on the slowing of the disease progression could provide more
decisive answers on how relevant high homocysteine and low folate
concentrations are to the onset and course of [Alzheimer’s disease] and
[vascular dementia].

(Quadri, Ex. 2009, 121.)
According to Nutricia, the statements are merely an indication of certain
insufficiencies in subjects with cognitive defects, not teachings that the subjects
would benefit from supplementation that the compounds. (See Nutricia Motion 1,
Paper 26, 11:1–7.) We agree that Quadri does not provide explicit direction to
treat persons having the characteristics of prodromal dementia by administering a
B-vitamin, but Quadri need not provide an express teaching for the method of
Count 1 to render it obvious to include B-vitamin in Nutricia’s method of
preventing or delaying the onset of dementia in persons with prodromal dementia.
Instead, the analysis of obviousness “need not seek out precise teachings directed
to the specific subject matter of the challenged claim, for a court can take account
of the inferences and creative steps that a person of ordinary skill in the art would
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employ.” KSR Int'l Co. v. Teleflex Inc., 550 U.S. 398, 418 (2007). Nutricia does
not direct us to evidence, such as testimony, showing that the suggestion that B-
vitamin deficiency precedes progression to Alzheimer’s disease and vascular
dementia would not have suggested to one of ordinary skill in the art that treatment
with B-vitamins could prevent or delay progression in those with characteristics of
prodromal dementia. Although MIT also fails to direct us to testimony in support
of its arguments, it is Nutricia’s burden to show that a skilled artisan seeking to
prevent or delay the onset of dementia would not have considered it obvious to
include B-vitamins with the composition of Count 1 from the teachings of Quadri.
(See MIT Opp. 1, Paper 51, 8:18–9:19.)
We note that the specification of Nutricia’s involved ’458 patent states:
“Advantageously, vitamin B12 and folate are included because low plasma
B12/folate levels are a risk factor for the development of [Alzheimer’s disease].”
(’458 patent, Ex, 2002, 9:7–10.) This statement echoes the results found in Quadri,
which was published several years earlier. (See Quadri, Ex. 2009, 120 (“The
results of the current cross-sectional study seem to indicate that relative folate
deficiency may already be present before the onset of dementia and, more
generally, may represent a risk factor for cognitive decline in the elderly.”).)
Nutricia argues further that the composition of claim 9 is not obvious over
Count 1 because it leads to unexpected results. (See Nutricia Motion 1, Paper 26,
12:18–18:7.) According to Nutricia, the addition of B-vitamins to the composition
of claim 1 of its involved ’458 patent leads to a significant and synergistic decrease
in the activity of a specific enzyme thought to be associated with dementia. (See
Nutricia Motion 1, Paper 26, 13:22–15:7.) In support, Nutricia presents a
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declaration by Nik van Wijk, who testifies that he is a Senior Scientist at Nutricia.
(See Declaration under 37 C.F.R. §1.132 (“van Wijk Decl.”), Ex. 2011, ¶ 1.)
According to Dr. van Wijk, reduction in gamma-secretase activity leads to a
reduction of amyloid beta peptides, which are thought to cause neural dysfunction
and neuronal death in Alzheimer’s disease. (See van Wijk Decl., Ex. 2011, ¶ 5.)
Dr. van Wijk reports that along with the inventors named on the ’458 patent, he
conducted a study of the effects of B-vitamins in diets comprising choline, an
omega 3 fatty acid (DHA) and a uridine monophosphate (UMP) (the components
of the compositions recited in Nutricia claim 1 and Count 1) that were also
enriched in B-vitamins. (See van Wijk Decl., Ex. 2009, ¶¶ 5–10.) Dr. van Wijik
describes four groups of rats, wherein
Group I received a control diet (B vitamin deficient and without DHA +
UMP). Group 2 received a B-vitamin deficient, DHA + UMP enriched diet.
Group 3 received a diet supplemented with B vitamins that did not contain
DHA +UMP. Group 4 received a diet supplemented with B vitamins and
enriched in DHA + UMP. All diets comprised choline at AIN-93M levels,
i.e. 1.0 g/kg diet (0.1 %)[ ].

(van Wijk Decl., Ex. 2011, ¶ 6 (citation omitted).) Dr. van Wijk reports that the B-
vitamin supplemented diets given were enriched with vitamin B6, vitamin B12,
and folic acid. (See van Wijk Decl., Ex. 2011, ¶ 7.)
Dr. van Wijk reports the results of gamma-secretase activity after four weeks
“of intervention,” demonstrated as the “rate of fluorescent signal increase caused
by peptide breakdown” measured with “a fluorescent assay using a gamma-
secretase specific peptide.” (See van Wijk Decl., Ex. 2011, ¶ 8.) These results are
reported in Figure 1 of Dr. van Wijk’s declaration, which is reproduced below.
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(van Wijk Decl., Ex. 2011, ¶ 9.) Dr. van Wijk summarizes these results:
This experiment demonstrate[s] that gamma-secretase activity was
significantly decreased in animals receiving the diet both enriched in B-
Vitamins and containing choline+DHA+UMP (-23% as compared to control
animals on the diet without B-vitamin and DHA+UMP supplementation,
p < 0.05). Supplementation of only DHA+UMP or only B-vitamins had no
significant effect on gamma-secretase activity. Hence, both B-vitamins and
DHA and/or UMP are required for a gamma-secretase lowering effect.

(van Wik Decl., Ex. 2011, ¶ 10.) According to Dr. van Wijk, these results show
that B-vitamins, added to a diet comprising choline, UMP and omega 3 fatty acids
(DHA) “have a synergistic effect on lowering the activity of gamma-secretase,
which in turn has been shown to result in a reduction of amyloid beta peptides,
which in turn has been how to translate to improved brain function in vivo[ ]. (van
Wik Decl., Ex. 2011, ¶ 11 (citation omitted).)
We are not persuaded that these results show the method recited in Nutricia
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claim 9 demonstrates would have been provided results that are unexpected over
the method of Count 1. First, the results presented by Dr. van Wijk are not
commensurate in scope with Nutricia claim 9. See In re Grasselli, 713 F.2d 731,
743 (Fed. Cir. 1983) (“[i]t is well settled ‘that objective evidence or non-
obviousness must be commensurate in scope with the claims which the evidence is
offered to support.’” (quoting In re Tiffin, 448 F.2d 791 (CCPA 1971))). Claim 9
recites “wherein the composition further comprises one or more B vitamins,”
without limiting the specific type of B-vitamin(s). Thus claim 9 encompasses all
B-vitamins. MIT argues that in addition to vitamin B6, vitamin B12, and folate,
which were tested by Dr. van Wijt, there are five other B-vitamins: B1, B2, B3,
B5, B7, and B9. (See MIT Opp. 1, Paper 51, 10:15–11:5.) Because the results
shown in Figure 1 of Dr. van Wijt’s declaration report decreased gamma-secretase
activity with a combination of only three B-vitamins, it fails to show that the full
scope of claim 9 would produce unexpected results.
In addition, we are unclear of the actual results presented because Dr. van
Wijk presents contradictory and confusing descriptions of the diets administered to
the groups of rats. In the text, Dr. van Wijk describes Groups 1 and 2 to have
received a “B-vitamin deficient” diet (van Wijk Decl., Ex. 2011, ¶ 6), but Figure 1
reports that the corresponding diets were “B-vitamin low” (van Wik Decl.,
Ex. 2011, ¶ 10). Adding to the confusion, Nutricia refers to these diets as
“moderately B-vitamin deficient” when discussing the results in Motion 1. (See
Nutricia Motion 1, Paper 26, 14:5–10.) Although Dr. van Wijt reported the
amounts of B-vitamins in the supplemented diets, it is unclear how they compared
to the amounts of B-vitamins in the groups meant to be controls. It is unclear
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whether the experiments show the result of the presence of B-vitamins or the effect
of a certain amount of B-vitamins, a limitation not included in claim 9.
In general, we are not persuaded that the effect seen in Figure 1 is
synergistic. To the extent we understand it, Dr. van Wijk determines that the
results are synergistic because only the combination of B-vitamins, DHA, and
UMP produced statistically significant results, with a p-value of less than 0.05.
(See van Wijk Decl., Ex. 2011, ¶ 10.) Dr. van Wijt determined this statistical
significance by comparing the gamma-secretase activity of Group 4 (choline,
DHA, and UMP supplemented with B-vitamin) to the activity of Group 1 (choline
and “low” or “deficient” B-vitamin). (See van Wijt declaration, Ex. 2011, ¶ 10.)
This is the wrong comparison for a determination of whether claim 9 corresponds
to Count 1.
Because the determination of correspondence to a count is a comparison
between the subject matter of the count and the claim, to determine if claim 9,
which adds B-vitamin to the composition, corresponds to Count 1, one must
compare the effect of a diet with and without B-vitamin as the only variable. That
is, the correct comparison is between a diet with an omega 3 fatty acid (DHA), a
uridine phosphate (UMP) and choline with B-vitamin (Group 4) to the effect of a
composition of DHA, UMP, and choline alone (Group 2).
Nutricia does not present any evidence that the difference in gamma-
secretase activity between Group 4 and Group 2 was statistically significant or
unexpected. Dr. van Wijt failed to report the underlying data for each group, but
Figure 1 does not seem to show a significant difference between Groups 2 and 4
because the bars, including the assigned error, appear to overlap. (See MIT Opp. 1,
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Paper 51, 13:1–10.) Accordingly, the results reported by Dr. van Wijt do not show
that including B-vitamin in a composition comprising DHA, UMP, and choline had
any unexpected effect on gamma-secretase activity.
Nutricia cites Example 4 of the specification of its involved ’458 patent in
support of the unexpected results allegedly demonstrated by Dr. van Wijt. (See
Nutricia Motion 1, Paper 26, 16:14–17:11.) We are not persuaded that Example 4
demonstrates that claim 9 recites a method having results that are unexpected over
the method of Count 1. Example 4 provides results from a comparison between
young mice reported to be at risk for Alzheimer’s disease that are fed a diet
without DHA, UMP, choline, or B-vitamin (“Diet A”) and the mice fed a diet with
all of those components (“Diet C”). (See ’458 patent, Ex. 2002, 11:47–12:29; see
Nutricia Motion 1, Paper 26, 16:20–17:3.) As discussed above in regard to the
experiment reported by Dr. van Wijt, this is the wrong comparison for a
consideration of whether claim 9 corresponds to Count 1. Because Count 1 recites
administering a composition of omega 3 fatty acid, a uridine phosphate, and a
choline salt, the correct comparison to show unexpected results would be of that
composition with and without B-vitamin. Accordingly, the results of a significant
decrease in neurodegeneration in mice fed Diet C in Example 4 of the ’458 patent
does not persuade us that Nutricia’s claim 9 demonstrates unexpected results
indicating it does not correspond to Count 1.
We are similarly not persuaded by the evidence Nutricia presents for the first
time in its Reply Brief. (See Nutricia Reply 1, Paper 76, 7:17–8:4, citing
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Jernerén9.) Like the experiment reported by Dr. Wijt and Example 4 of the
’458 patent, the study reported in Jernerén does not compare patients administered
omega-3 fatty acid, a uridine phosphate and choline with and without B-vitamin.
Instead, Jernerén compares the effects of omena-3 fatty acid and DHA separately,
with and without B-vitamin. Jernerén reports that there was “a significant
interaction between B vitamin treatment and combined v-3 (P = 0.024) . . . ,” but
that “[t]he interaction was not significant for DHA (P = 0.134).” (Jernerén,
Ex. 2022, 4.) Nutricia does not provide the testimony of one of ordinary skill in
the art or of an expert witness as evidence of how these results would have been
understood. In the absence of such testimony, we cannot know if the results
indicate that the subject matter of claim 9 would have been unexpected over the
subject matter of Count 1. Accordingly, the evidence is not persuasive.
The preponderance of the evidence does not persuade us that the method of
Nutricia claim 9 demonstrates unexpected results over the subject matter of
Count 1 and we are not persuaded that the method of claim 9 would not have been
obvious over the method of Count 1. Accordingly, Nutricia has failed to persuade
us that claim 9 should be designated as not corresponding to Count 1.
Conclusion
Because Nutricia has failed to persuade us that either claim 2 or claim 9 of
its involved ’458 patent should be designated as not corresponding to Count 1, we
DENY Nutricia Motion 1.

9 Jernerén, et al., “Brain atrophy in cognitively impaired elderly: the importance of
long-chain v-3 fatty acids and B vitamin status in a randomized controlled trial,”
AM. J. CLIN. NUTR., doi:10.3945/ajcn.114.103283 (2015).
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As explained above, we decline to decide MIT Motions 1, 2, and 3 because
the issues they present are moot in light of Nutricia’s failure to assert a date of
priority earlier than MIT’s accorded benefit date. Therefore, we DISMISS MIT
Motions 1, 2, and 3.
Judgment against Nutricia, canceling all of the claims of the ’458 patent,
will be entered in a separate paper.

cc (via e-mail):
Attorney for Junior Party Nutricia
David R. Fairbairn
Alan M. Koenck
KINNEY & LANGE, P.A.
drfairbairn@kinney.com
amkoenck@kinney.com

Attorney for Senior Party MIT

Mark Cohen
Craig L. Puckett
PEARL COHEN ZEDEK LATZER BARATZ LLP
mcohen@pearlcohen.com
cpuckett@pearlcohen.com