Distinct clinical and metabolic deficits in
PCA and AD are not related to amyloid
M.H. Rosenbloom, MD
A. Alkalay, MD
S.L. Baker, PhD
J.P. O’Neil, PhD
M. Janabi, PhD
I.V. Yen, BA
M. Growdon, BA
J. Jang, BA
C. Madison, MA
E.C. Mormino, BS
H.J. Rosen, MD
M.W. Weiner, MD
B.L. Miller, MD
W.J. Jagust, MD
G.D. Rabinovici, MD
Background/Objective: Patients with posterior cortical atrophy (PCA) often have Alzheimer dis-
ease (AD) at autopsy, yet are cognitively and anatomically distinct from patients with clinical AD.
using Pittsburgh compound B (PiB) and FDG-PET.
Methods: Patients with PCA (n ? 12, age 57.5 ? 7.4, Mini-Mental State Examination [MMSE]
22.2 ? 5.1), AD (n ? 14, age 58.8 ? 9.6, MMSE 23.8 ? 6.7), and cognitively normal controls
(NC, n ? 30, age 73.6 ? 6.4) underwent PiB and FDG-PET. Group differences in PiB distribution
volume ratios (DVR, cerebellar reference) and FDG uptake (pons-averaged) were assessed on a
voxel-wise basis and by comparing binding in regions of interest (ROIs).
throughout frontal, temporoparietal, and occipital cortex (p ? 0.0001). There were no regional
differences in PiB binding between PCA and AD even after correcting for atrophy. FDG patterns
in PCA and AD were distinct: while both groups showed hypometabolism compared to NC in
temporoparietal cortex and precuneus/posterior cingulate, patients with PCA further showed hy-
pometabolism in inferior occipitotemporal cortex compared to both NC and patients with AD (p ?
0.05). Patients with AD did not show areas of relative hypometabolism compared to PCA.
Conclusions: Fibrillar amyloid deposition in PCA is diffuse and similar to AD, while glucose hypo-
metabolism extends more posteriorly into occipital cortex. Further studies are needed to deter-
mine the mechanisms of selective network degeneration in focal variants of AD. Neurology®2011;
AD ? Alzheimer disease; DVR ? distribution volume ratio; FWE ? family-wise error; LPA ? logopenic aphasia; MMSE ?
Mini-Mental State Examination; MNI ? Montreal Neurological Institute; NC ? normal control; NFT ? neurofibrillary tangle(s);
PCA ? posterior cortical atrophy; PiB ? Pittsburgh compound B; PPA ? primary progressive aphasia; ROI ? region of
interest; VBM ? voxel-based morphometry; VOSP ? Visual Object and Space Perception battery.
Posterior cortical atrophy (PCA) is a focal neurodegenerative disorder of higher visual process-
ing and spatial praxis with relative sparing of memory and insight.1At autopsy, the majority of
patients are found to have underlying Alzheimer disease (AD) as the causative pathology.1-3
The distribution of AD pathology in PCA is controversial, with some studies demonstrating
higher numbers of amyloid plaques in primary and association visual cortex in PCA compared
to typical AD4,5and others showing no difference in the distribution of A? pathology.2,3
Postmortem comparisons are limited in that they study the end stages of disease, which makes
relating changes seen at autopsy to in vivo disease evolution difficult.
Fibrillar A? pathology can be measured during life using PET with [11C]-labeled Pittsburgh
compound B (PiB-PET).6PiB binding during life correlates strongly with distribution and
e-Pub ahead of print on April 27, 2011, at www.neurology.org.
From the Memory and Aging Center and Department of Neurology (M.H.R., A.A., M.G., J.J., H.J.R., M.L.G.-T., B.L.M., W.J.J., G.D.R.),
University of California San Francisco, San Francisco; Helen Wills Neuroscience Institute (A.A., N.A., C.M., E.C.M., W.J.J., G.D.R.), University of
California Berkeley, Berkeley; Lawrence Berkeley National Laboratory (S.L.B., J.P.O., M.J., I.V.Y., W.J.J., G.D.R.), Berkeley; and Center for Imaging
of Neurodegenerative Diseases (M.W.W.), Department of Veterans Affairs Medical Center, San Francisco, CA.
Study funding: Supported by the NIH/NIA K23-AG031861, R01-AG027859, P01-AG1972403, P50 AG023501, Alzheimer’s Association NIRG-07-
59422, ZEN-08-87090, John Douglas French Alzheimer’s Foundation, and State of California DHS-ADRC 04-33516.
Disclosure: Author disclosures are provided at the end of the article.
Address correspondence and
reprint requests to Dr. Michael
HealthPartner Specialty Center,
Center for Dementia and
Alzheimer’s Care, 401 Phalen
Boulevard, Mail Stop: 41104C,
St. Paul, MN 55130
Copyright © 2011 by AAN Enterprises, Inc.
burden of fibrillar A? found at autopsy.7,8
Previous case reports have described increased
occipital PiB binding in individual patients
with PCA.9-11However, occipital PiB binding
is also seen in AD.6,12,13To our knowledge, no
study has directly compared PiB uptake at a
group level in PCA and AD.
Based on the preponderance of postmor-
tem data and previously demonstrated disso-
ciations between PiB binding and clinical
features of AD,14,15we hypothesized that pa-
tients with PCA would show diffuse cortical
PiB binding in a pattern indistinguishable
from clinically “typical” AD, but greater glu-
cose hypometabolism than patients with AD
in occipital cortex, correlating with their se-
lective impairment in visual processing.
METHODS Study population. Patients were recruited
from PCA and AD cohorts followed at the University of Califor-
nia San Francisco Memory and Aging Center. All patients un-
derwent a history and physical examination, a structured
caregiver interview, and neuropsychological tests.16Visuospatial
function was assessed using the modified Rey-Osterrieth design,
copy of intersecting pentagons, and the number location task
from the Visual Object and Space Perception battery (VOSP).17
Verbal memory was assessed using the 9-item California Verbal
Learning Test18and visual memory with recall of the modified
Rey-Osterrieth design. The remainder of the neuropsychological
test battery has been previously described.16Clinical diagnosis
was assigned by consensus at a multidisciplinary conference.
Medical records of patients clinically diagnosed with PCA
were reviewed by a neurologist (M.H.R.) blinded to PET data to
ensure they met the following criteria19: 1) presentation with
progressive visual or visuospatial impairment in the absence of
ophthalmologic impairment; 2) evidence of complex visual dis-
order on examination: elements of Balint syndrome, visual agno-
sia, dressing apraxia, or environmental disorientation; 3)
proportionately less memory loss. To meet criteria, patients were
required to present with early complaints of visuospatial impair-
ment in the absence of memory complaints. Impairments in
higher visual processing on neurologic examination were re-
quired. A neuropsychological profile showing predominant visu-
ospatial impairments with relative sparing of verbal episodic
memory (in the judgment of the investigator) was also obliga-
tory. Visual memory scores were not considered as these can be
impaired in PCA due to primary visuospatial dysfunction rather
than true memory loss. Structural MRI was reviewed to confirm
a pattern of posterior cortical atrophy involving visual associa-
tion areas. Subjects with early memory impairment, ophthalmo-
logic disease, extrapyramidal symptoms or signs, hallucinations,
cognitive fluctuations, or significant occipito-parietal MRI T2
white matter hyperintensities were excluded. Twelve eligible pa-
tients with PCA were enrolled in the study (table 1).
A comparison group of 14 patients meeting standard clinical
criteria for AD (National Institute of Neurological and Commu-
nicative Disorders and Stroke–Alzheimer’s Disease and Related
Disorders Association20) were selected to match the PCA cohort
for age, sex, and Mini-Mental State Examination (MMSE) score
(table 1). An imaging control group of 30 cognitively normal
older individuals (NC) were recruited from the community
(mean age ? 73.6 ? 6.4, 22 female, 8 male, mean education ?
17.7 ? 1.8 years).21All participants underwent PET imaging
between April 2005 and October 2009.
Standard protocol approvals, registrations, and con-
sents. The study was approved by the University of California
Berkeley, UCSF, and Lawrence Berkeley National Laboratory
institutional review boards for human research. Consent for the
study was provided by the participants or their assigned surro-
Image analysis. Image acquisition and preprocessing. All
subjects underwent PET imaging with [11C] PiB and [18F] FDG
at Lawrence Berkeley National Laboratory on a Siemens ECAT
EXACT HR PET scanner in 3-dimensional acquisition mode.
Tracer synthesis, PET acquisition, and preprocessing were per-
formed as previously described22(see appendix e-1 on the Neu-
Table 1Demographics and neuropsychological test scoresa
Age at onset, y
58.8 (9.6)57.5 (7.4)0.58
Age at PET, y
63.9 (9.1)62.3 (7.5) 0.62
Disease duration, y
5.0 (2.8) 4.8 (2.6) 0.79
17.0 (2.4) 16.0 (3.2)0.36
APOE4 (0, 1, 2)
3, 3, 55, 2, 2 0.41
21.9 (6.9)22.2 (5.1)0.87
CVLT-SF total learning (31.3 ? 2.4)
14.0 (6.6)19.9 (6.3) 0.06
CVLT-SF 10-min recall (7.9 ? 1.5)
1.4 (1.6)3.7 (3.3) 0.05
Modified Rey 10-min recall (12.4 ? 2.7)
2.6 (2.5) 4.2 (4.5)0.30
Modified Rey Copy (15.6 ? 1.1)
11.8 (4.7) 7.6 (5.8) 0.06
VOSP spatial location test (9.2 ? 1.01)
7.6 (2.7)5.4 (2.5) 0.07
Modified Trails B time (27.1 ? 11.5)
97.8 (34.5)105.6 (15.7)0.56
Modified Trails B no. correct lines (14 ? 0)
9.8 (5.9)6.5 (6.0)0.78
Digit backward span (5.4 ? 1.3)
3.0 (1.4) 3.3 (0.9) 0.75
Stroop interference test no. correct
(56.6 ? 12.3)
18.0 (12.3)24.1 (18.2)0.44
Boston Naming Test (14.5 ? 0.9)
10.8 (4.0) 11.8 (3.7)0.57
Syntax comprehension (5 ? 0)
3.1 (1.0)3.0 (1.6) 0.85
Letter fluency (D words) (16.8 ? 4.2)
10.6 (6.1)10.8 (4.3) 0.92
Category fluency (animals) (24.7 ? 4.5)
8.8 (4.6) 12.0 (6.3) 0.16
Calculations (4.8 ? 0.7)
3.4 (1.4)3.2 (1.1) 0.63
CDR sum of boxes
5.3 (3.8)3.8 (2.9) 0.26
Verbal Learning Test; MMSE ? Mini-Mental State Examination; PCA ? posterior cortical
atrophy; VOSP ? visual object and space perception.
aAge-matched normative values listed in parenthesis beside each test. Group values are
shown as mean (SD).
Neurology 76 May 24, 2011
rology®Web site at www.neurology.org for details). One patient
with PCA did not undergo FDG due to technical reasons.
For PiB, voxel-wise distribution volume rations were calcu-
lated using Logan graphical analysis, with the cerebellum time-
activity curve used as a reference tissue input function (t ?
35–90 minutes).23,24FDG frames for each subject were summed
and normalized to mean activity in the pons.25
Given the differential atrophy patterns seen in AD and PCA,26
we corrected PET data for atrophy by applying a 2-compartmental
12/14 AD, and all NC) (see appendix e-1).15,27Since the benefit of
partial volume correction for PiB data are controversial, all primary
analyses were performed using uncorrected PET data, while confir-
matory analyses were conducted with atrophy-corrected data in the
subset of patients with an MRI.
Voxel-wise group comparisons. Individual subject PiB and
FDG volumes were spatially normalized to Montreal Neurolog-
ical Institute (MNI) space using SPM 5 (see appendix e-1).15All
normalized images were smoothed with a 12-mm kernel. Voxel-
wise comparisons of PiB distribution volume ratio and pons-
normalized FDG images were performed in an analysis of
covariance model that included diagnosis (PCA, AD, NC) as the
condition and education and sex as covariates. Pairwise contrasts
were performed among the 3 groups. To allow broad visualiza-
tion of the data, results were displayed on a template brain as
T-maps thresholded at p ? 0.001 uncorrected for multiple
comparisons. Voxels were considered significant at p ? 0.05
after family-wise error (FWE) correction for AD/PCA vs NC
contrasts, and at p ? 0.001 uncorrected for direct AD vs PCA
Region of interest definition. PET values were extracted in
normalized space from regions of interest (ROIs) derived from
the Automated Anatomic Labeling Atlas.28A custom ROI was
created by generating 10-mm spheres around the peak voxel de-
tected in right lateral occipitotemporal cortex in a previous study
contrasting gray matter volumes in PCA and AD (MNI coordi-
nates x ? 39, y ? ?85, z ? ?6)29and the corresponding voxel
in the left hemisphere.
To represent tracer binding in occipital cortex relative to
global PiB or FDG uptake, an occipital percentage (occipital pct)
was calculated: Occipital pct ? (mean occipital PiB or FDG)/
(mean cortical PiB or FDG).
Statistical analysis. Group differences in continuous variables
were examined using t tests or one-way analysis of variance and
Tukey post hoc contrasts. Differences in dichotomous variables
were measured using Pearson ?2.
RESULTS Subject characteristics. By design, pa-
tients with PCA and patients with AD were well-
matched for age, education, and disease severity
(table 1). NC were older than the patients (p ?
0.0001) but were matched for sex and education.
The APOE ?4 genotype was more common in pa-
tients with AD than controls (p ? 0.02), but there
was no difference in frequency between PCA
On neuropsychological testing, patients with AD
performed more poorly on verbal memory tests (p ?
0.05, table 1) and patients with PCA showed nonsig-
nificant trends toward worse performance on visu-
ospatial tasks (p ? 0.06 for Rey copy, p ? 0.07 for
VOSP number location). No differences were found
on tests of executive function or language.
All clinically diagnosed patients with PCA and
patients with AD showed increased global PiB bind-
ing compared to controls on visual inspection, sup-
porting the assumption of underlying AD pathology.
None of the subjects have undergone autopsy.
PiB: Voxel-wise comparisons. Compared to NC, both
patients with AD and patients with PCA showed dif-
fuse, symmetric PiB binding throughout cortex with
sparing of primary sensorimotor and visual areas and
hippocampus (p [FWE] ?0.05, figure 1). There
were no regions of increased PiB binding in the
PCA ? AD condition at a threshold of p ? 0.001
uncorrected. In the AD ? PCA comparison, small
clusters of elevated binding were seen in pons and
cerebellum at p ? 0.001 uncorrected, but these were
not considered significant as they were not located in
regions that showed elevated PiB in AD vs NC.
PiB: ROI comparisons. Both AD and PCA groups
had significantly higher PiB uptake throughout all
ROIs in comparison to NC (p ? 0.001, table e-1)
except in hippocampus in which a significant differ-
ence was detected only between AD and NC (p ?
0.05). There were no differences in PiB uptake be-
tween AD and PCA in any ROIs or in the occipital
pct (0.93 ? 0.08 in PCA, 0.91 ? 0.07 in AD, p ?
0.81, figure 2). Following atrophy correction, there
was a trend for higher PiB in PCA compared to AD
in cuneus and lingual gyrus (p ? 0.09 for both) but
not in other ROIs or in occipital pct (0.91 ? 0.07 in
PCA, 0.86 ? 0.09 in AD, p ? 0.26).
FDG: Voxel-wise comparisons. Compared to NC,
both patient groups showed hypometabolism in bi-
lateral angular gyrus, middle and inferior temporal
gyrus, and inferior parietal lobule, with hypometabo-
lism in PCA extending posteriorly to bilateral infe-
rior, middle, and superior occipital gyrus, precuneus,
and right calcarine cortex (p [FWE] ?0.05, figure 1).
When directly compared to AD, patients with PCA
showed relative hypometabolism in bilateral fusiform
gyrus, inferior, middle, and superior occipital gyrus, left
lingual gyrus, right inferior temporal cortex, bilateral
parisons correction. There were no regions of relative
FDG: ROI comparisons. Compared to NC, FDG up-
take was decreased bilaterally in both PCA and AD
throughout lateral temporoparietal cortex, precu-
neus, inferior and middle occipital gyrus, and the lat-
eral occipitotemporal ROI (p ? 0.05, table e-2).
Neurology 76May 24, 2011
Subjects with PCA alone showed hypometabolism in
bilateral fusiform gyrus, cuneus, superior occipital,
and left lingual gyrus (p ? 0.05). These findings re-
mained significant after atrophy correction (p ?
0.05). Compared to AD, patients with PCA showed
lower FDG in the lateral occipitotemporal cortex,
inferior, middle, and superior occipital gyrus, and
right cuneus (p ? 0.05, figure 2). Following atrophy
correction, there was lower metabolism in PCA rela-
tive to AD in bilateral inferior occipital cortex and
the lateral occipitotemporal ROI (p ? 0.05). Pre-
atrophy and post-atrophy correction, the FDG oc-
cipital pct in PCA (0.92 ? 0.06 pre-atrophy
correction, 0.93 ? 0.05 post-correction) was lower
than in AD (1.06 ? 0.13 pre-atrophy, 1.02 ? 0.14
post-correction, p ? 0.05 for both) and NC (1.07 ?
0.04 pre-atrophy, 1.04 ? 0.04 post-atrophy correc-
tion, p ? 0.05 for both). There were no regions of
hypometabolism in AD relative to PCA.
DISCUSSION In this study we compared clinical
features, fibrillar A? deposition, and regional glucose
metabolism in matched patients presenting clinically
with PCA and AD. As expected, patients with PCA
showed greater impairment in visuospatial tasks and
patients with AD showed relative deficits in episodic
memory. All patients with PCA showed high PiB
uptake, consistent with previous reports that the clin-
ical syndrome of PCA is very often associated with
underlying AD pathology.1-3The pattern of cortical
PiB binding in PCA was diffuse, affecting anterior
and posterior cortical regions, visual and nonvisual
areas, and on direct statistical comparison was indis-
tinguishable from the pattern seen in AD. In con-
trast, patients with PCA showed a more posterior
pattern of glucose hypometabolism with greater oc-
cipital involvement than was seen in patients with
clinically “typical” AD. These findings suggest that
distinct clinical features and regional hypometabo-
lism in PCA and AD are not related to fibrillar amy-
Previous autopsy studies have yielded conflicting
results regarding the distribution of amyloid pathol-
Figure 1 Patterns of Pittsburgh compound B (PiB) and FDG binding in Alzheimer disease (AD) and posterior cortical atrophy (PCA)
compared to normal controls (NC) and to each other
T-score maps are rendered on the ch2 template brain. All results are presented at a threshold of p ? 0.001, uncorrected for multiple comparisons.
Neurology 76 May 24, 2011
ogy in PCA, with some studies reporting 3–5 times
more plaques in visual areas in patients with PCA
compared to patients with typical AD,5and others
finding similar plaque counts in these regions in PCA
and AD.2,3The reasons for these discrepant findings
are unclear, but may include subject factors (e.g., age,
disease severity, failure to control for copathology) as
well as the methods used to quantify plaques (e.g.,
lesion counts vs more rigorous quantification, stain-
ing techniques, discrimination between diffuse vs
neuritic plaques). Our data suggest that, in the mild-to-
moderate disease stage, there is no difference in the dis-
tribution of fibrillar A? pathology between PCA and
AD. These findings are congruent with observations
from patients with underlying AD who present with
another focal cortical syndrome, primary progressive
aphasia (PPA). Though neurodegeneration in PPA is
highly asymmetric and preferentially involves the
language network,30,31the distribution of amyloid pa-
thology (as measured by PiB or at autopsy) in AD-
associated cases is symmetric and indistinguishable
from that found in typical AD.14,32
Previously, our group used voxel-based morphome-
early age-at-onset AD, PCA, and logopenic aphasia
(LPA), a PPA variant associated with underlying AD.31
We found that patients with all 3 syndromes showed
overlapping atrophy in precuneus/posterior cingulate
and lateral temporoparietal cortex. Additional right
ventral-occipital/parietal atrophy was found in PCA
and left middle/superior temporal gyrus atrophy in
LPA. Similar results were reported in another study
contrasting atrophy patterns in AD and PCA.31Like-
wise, in this study we found comparable glucose hypo-
metabolism in AD and PCA in temporoparietal cortex
and precuneus, with extension of hypometabolism into
occipitotemporal cortex in PCA. These observations
suggest that precuneus/posterior cingulate and lateral
temporoparietal involvement is a common feature of
AD-associated syndromes, with extension of neurode-
It is intriguing to speculate whether common involve-
ment of these regions in AD is related to their proposed
function as highly interconnected “cortical hubs,”
Figure 2 Box plots representing pre-atrophy and post-atrophy Pittsburgh compound B (PiB) and FDG uptake for the lateral
occipitotemporal region and occipital percentage (ratio of occipital to global cortical PiB/FDG)
*Less than Alzheimer disease (AD) and posterior cortical atrophy (PCA), p ? 0.05. **Greater than AD and PCA, p ? 0.05. †Less than normal controls (NC), p ?
0.05. ‡Less than AD and NC, p ? 0.05.
Neurology 76May 24, 2011
which may render them susceptible to both early A?
A? release) and A?-mediated neurodegeneration (due
tivity may also enable the spread of disease from these
regions into several cortical networks,34including those
underlying memory, language, and visual function.
Our work in early-onset AD,15PPA,14and now PCA
suggests that the respective involvement of these net-
works is not explained by the distribution of amyloid.
Rather, it may be the relative vulnerability of networks
in an individual that determines the neurodegenerative
pattern and clinical phenotype of AD. In most patients
the posterior “default mode network” may be most vul-
nerable to A?-mediated neurodegeneration, perhaps
because of high metabolic demand,35leading to a “typi-
cal” amnestic AD phenotype. In individuals with PPA,
however, the language network may be particularly vul-
nerable, as suggested by the high rate of developmental
have not been systematically studied in PCA, where vi-
sual networks are disproportionately affected. Future
studies that estimate premorbid “reserve” in specific
cognitive domains, investigate the integrity and func-
tion of the associated neural networks, and relate these
findings to clinical and degenerative phenotype may
help elucidate the mechanisms of selective network de-
generation in focal variants of AD.
Another possible explanation for the dissociation
between the patterns of PiB and FDG binding in this
study is that the fibrillar A? deposits imaged by PiB
may not be the critical pathology driving neurode-
generation. Soluble A? oligomers are considered to
be the most neurotoxic A? species,37,38yet are not
bound by PiB. It is possible the patients with PCA
have high concentrations of A? oligomers in visual
areas, though it is not clear why this would not be
reflected by higher concentrations of fibrillar A? that
is thought to be in equilibrium with the soluble com-
partment. Finally, the degenerative pattern is likely
more closely related to the distribution of neurofi-
counts in visual regions in PCA compared to AD is a
consistent finding across pathology studies,2,3,5and
unknown, however, whether in AD NFT form inde-
pendently or secondary to A?-driven processes.
most subjects with PCA in our cohort showed diffuse
PiB binding, individual subjects with posterior-
predominant binding patterns could be identified,
though conversely frontal-predominant binding was
seen in one subject, and similar variability in binding
patterns was also seen in the “typical” AD group. Fol-
lowing atrophy correction, there was a trend toward
higher mean PiB values for PCA compared to AD in
the cuneus and lingual gyrus (p ? 0.09), leaving open
the possibility that subtle increases in occipital amyloid
3- to 5-fold higher magnitude reported in some pathol-
inflation of PET counts by the atrophy correction
procedure, which remains controversial for PiB data.
lism in PCA compared to AD showed essentially iden-
tical PiB uptake in the 2 groups even after atrophy
correction (e.g., lateral occipitotemporal and inferior
occipital cortex), supporting the assertion that PiB and
FDG patterns are dissociated in the 2 syndromes.
Our study has limitations. The sample sizes were
relatively small, potentially limiting our power to detect
differences between AD and PCA, though the size of
our cohorts is comparable to those found in previous
studies of PCA, and had sufficient power to detect dif-
ferences in FDG binding and marginal differences in
clinical performance. Although initial studies suggest
tem A? measures,11,8the limitations of this technique
have not yet been fully identified. It is possible that pa-
in addition to AD, though this is less likely given the
exclusion of subjects with clinical features suggestive of
dementia with Lewy bodies, corticobasal degeneration,
or prion disease. Since we matched the AD and PCA
groups for age, our AD control group is largely com-
posed of early age-at-onset patients (mean age at onset
anatomic differences between AD and PCA, since pa-
tients with early-onset AD have greater visuospatial im-
pairment and posterior cortical atrophy and relatively
preserved episodic memory and medial temporal lobes
compared to late-onset patients.39,40
Dr. Rosenbloom, A. Alkalay, N. Agarwal, and Dr. Baker report no disclo-
sures. Dr. O’Neill receives research support from Genzyme Corporation,
the US Department of Energy, the US Army Medical Research & Mate-
riel Command, and the NIH. Dr. Janabi receives research support from
the NIH. I.V. Yen, M. Growdon, J. Jang, C. Madson, and E.C. Mormino
report no disclosures. Dr. Rosen serves on a scientific advisory board for
Avanir Pharmaceuticals; receives publishing royalties for The Emotional
Brain (Oxford University Press); and receives research support from the
NIH (NIA, NINDS, DHS/ADP/ARCC) and the Larry L. Hillblom
Foundation. Dr. Gorno-Tempini receives research support from the NIH
(NINDS, NIA), the John Douglas French Alzheimer’s Foundation, the
Neurology 76 May 24, 2011
Alzheimer’s Association, the Larry L. Hillblom Foundation, the Koret
Family Foundation, and the McBean Family Foundation. Dr. Weiner
serves on scientific advisory boards for Bayer Schering Pharma, Eli Lilly
and Company, CoMentis, Inc., Neurochem Inc, Eisai Inc., Avid Radio-
pharmaceuticals Inc., Aegis Therapies, Genentech, Inc., Allergan, Inc.,
Lippincott Williams & Wilkins, Bristol-Myers Squibb, Forest Laborato-
ries, Inc., Pfizer Inc, McKinsey & Company, Mitsubishi Tanabe Pharma
Corporation, and Novartis; has received funding for travel from Nestle ´
and Kenes International and to attend conferences not funded by indus-
try; serves on the editorial board of Alzheimer’s & Dementia; has received
honoraria from the Rotman Research Institute and BOLT International;
serves as a consultant for Elan Corporation; receives research support from
Merck & Co., Radiopharmaceuticals Inc., the NIH, the Veterans Admin-
istration, and the State of California; and holds stock in Synarc and Elan
Corporation. Dr. Miller serves on a scientific advisory board for the Alz-
heimer’s Disease Clinical Study; serves as an Editor for Neurocase and as
an Associate Editor of ADAD; receives royalties from the publication of
Behavioral Neurology of Dementia (Cambridge, 2009), Handbook of Neu-
rology (Elsevier, 2009), and The Human Frontal Lobes (Guilford, 2008);
serves as a consultant for Lundbeck Inc., Elan Corporation, and Allon
Therapeutics, Inc.; serves on speakers’ bureaus for Novartis and Pfizer
Inc.; and receives research support from Novartis and the NIH/NIA and
the State of California Alzheimer’s Center. Dr. Jagust has served on a
scientific advisory board for Genentech, Inc.; serves as Associate Editor for
Frontiers in Human Neuroscience and on the editorial boards of Annals of
Neurology, Brain Imaging and Behavior, and Alzheimer’s Disease and Asso-
ciated Disorders; receives publishing royalties for Imaging the Aging Brain
(Oxford University Press, 2009); has served as a consultant for Synarc,
Elan Corporation/Janssen Alzheimer Immunotherapy, Genentech, Inc.,
Abbott, GE Healthcare, Ceregene, Bayer Schering Pharma, Schering-
Plough Corp., TauRx Pharmaceuticals, Otsuka Pharmaceutical Co., Ltd.,
and Merck & Co; and receives research support from the NIH and from
the Alzheimer’s Association. Dr. Rabinovici serves on scientific advisory
boards for Novartis and GE Healthcare and receives research support
from the NIH/NIA, the Alzheimer’s Association, and the John Douglas
French Alzheimer’s Foundation.
Received August 9, 2010. Accepted in final form November 23, 2010.
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