34th Annual

International Conference
of the IEEE Engineering in
Medicine and Biology Society
28 August - 1 September, 2012 San Diego, CA USA
Conference Chair: Michael C.K. Khoo
Program Co-Chairs: Gert Cauwenberghs and James D. Weiland

U.S. National Library of Medicine

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United States National Library of Medicine

Welcome Keynote Speakers

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08:30-08:45 SaA01.3
Gaussian Process Regression in Vital-Sign Early Warning Systems ............................................................ 6161-6164
Clifton, Lei* (University of Oxford); Clifton, David (University of Oxford); Pimentel, Marco A.F. (University of
Oxford); Watkinson, Peter J. (University of Oxford, Oxford University Hospitals NHS Trust);
Tarassenko, Lionel (University of Oxford)

08:45-09:00 SaA01.4
Extraction of Fetal Heart Rate from Maternal Surface ECG with Provisions for Multiple Pregnancies ...... 6165-6168
Fanelli, Andrea (Politecnico di Milano); Signorini, Maria G.* (Politecnico di Milano);
Heldt, Thomas (Massachusetts Institute of Technology)

09:00-09:15 SaA01.5
Determination of Glucose Concentration from Near-Infrared Spectra Using Locally Weighted Partial
Least Square Regression .................................................................................................................................... 6169-6171
Malik, Bilal* (Sheffied University); Benaissa, Mohammed (Sheffied University)

09:15-09:30 SaA01.6
Multivariate Spectral Analysis for Identifying the Brain Activations During Olfactory Perception ............ 6172-6175
Kroupi, Eleni* (EPFL); Yazdani, Ashkan (EPFL); Vesin, Jean-Marc (EPFL); Ebrahimi, Touradj (EPFL)

SaA02: 08:00-09:30 Sapphire D

1.5.1 Casuality and Connectivity (Oral Session)
Chair: Tong, Shanbao (Shanghai Jiao Tong Univ.)
Co-Chair: Porta, Alberto (Univ. degli Studi di Milano)

08:00-08:15 SaA02.1
An Association Framework to Analyze Dependence Structure in Time Series ............................................ 6176-6179
Fadlallah, Bilal* (University of Florida); Brockmeier, Austin (University of Florida); Seth, Sohan
(University of Florida); Keil, Andreas (University of Florida); Principe, Jose (University of Florida)

08:15-08:30 SaA02.2
On the Improved Correlative Prediction Scheme for Aliased Electrocardiogram
(ECG) Data Compression .................................................................................................................................... 6180-6183
Gao, Xin* (The University of Arizona, Tucson)

08:30-08:45 SaA02.3
Comparing Causality Measures of Fmri Data Using PCA, CCA and Vector Autoregressive Modelling ..... 6184-6187
Shah, Adnan* (National ICT Australia, Canberra, The Australian National University Canberra); Khalid,
Muhammad Usman (National ICT Australia, Canberra, The Australian National University Canberra);
Seghouane, Abd-krim (National ICT Australia)

08:45-09:00 SaA02.4
Synchrony Analysis of Spontaneous MEG Activity in Alzheimer’s Disease Patients .................................. 6188-6191
Gomez, Carlos* (University of Valladolid, CIF: Q4718001C); Martínez-Zarzuela, Mario (Grupo de Telemática
Industrial, University of Valladolid); Poza, Jesús (University of Valladolid); Díaz-Pernas, Francisco Javier (Grupo
de Telemática Industrial, University of Valladolid); Fernandez, Alberto (Universidad Complutense de Madrid);
Hornero, Roberto (University Of Valladolid)

09:00-09:15 SaA02.5
Towards the Time Varying Estimation of Complex Brain Connectivity Networks by Means of a General
Linear Kalman Filter Approach ........................................................................................................................... 6192-6195
Astolfi, Laura* (University of Rome Sapienza); Toppi, Jlenia (University of Rome “Sapienza”)

09:15-09:30 SaA02.6
Cortical Functional Connectivity under Different Auditory Attentional Efforts ............................................ 6196-6199
Hong, Xiangfei (Shanghai Jiao Tong University); Tong, Shanbao* (Shanghai Jiao Tong University)
34th Annual International Conference of the IEEE EMBS
San Diego, California USA, 28 August - 1 September, 2012
Synchrony analysis of spontaneous MEG activity in
Alzheimer’s disease patients
Carlos Gómez*, Member, IEEE, Mario Martínez-Zarzuela, Jesús Poza, Member, IEEE,
Francisco J. Díaz-Pernas, Alberto Fernández, and Roberto Hornero, Senior Member, IEEE
Abstract— The aim of this study was to analyze the
magnetoencephalography (MEG) background activity in
Alzheimer’s disease (AD) patients using cross-approximate
entropy (Cross-ApEn). Cross-ApEn is a nonlinear measure of
asynchrony between time series. Five minutes of recording
were acquired with a 148-channel whole-head magnetometer in
12 AD patients and 12 age-matched control subjects. We found
significantly higher synchrony between MEG signals from AD
patients compared with control subjects. Additionally, we
evaluated the ability of Cross-ApEn to discriminate these two
groups using receiver operating characteristic (ROC) curves
with a leave-one-out cross-validation procedure. We obtained
an accuracy of 70.83% (66.67% sensitivity, 75% specificity)
and a value of area under the ROC curve of 0.83. These results
provide evidence of disconnection problems in AD. Our
findings show the usefulness of Cross-ApEn to detect the brain
dysfunction in AD.
I. INTRODUCTION
A LZHEIMER’S DISEASE (AD) is a primary degenerative
neurological disorder of unknown etiology that
gradually destroys brain cells. Nowadays, it is considered
the main cause of dementia in western countries [1]. AD
affects 1% of population aged 60-64 years, but the
prevalence increases exponentially with age, so about 30%
of people over 85 years suffer from this disease [2].
Additionally, as life expectancy has improved significantly
in the last decades, it is expected that the number of people
with dementia increase up to 81 millions in 2040 [2].
Clinically, this disease manifests as a slowly progressive
impairment of mental functions whose course lasts several
years prior to death [2]. Usually, AD starts by destroying
neurons in parts of the patient’s brain that are responsible for
storing and retrieving information. Then, it affects the brain
areas involved in language and reasoning. Eventually, many
other brain regions are atrophied. Although a definite AD
diagnosis is only possible by necropsy, a differential
diagnosis with other types of dementia and with major
Manuscript received March 29, 2012. This research was supported in
part by the “Ministerio de Economía y Competitividad” under project
TEC2011-22987, the Proyecto Cero 2011 on Ageing from Fundación
General CSIC, and project VA111A11-2 from Consejería de Educación
(Junta de Castilla y León). Asterisk indicates corresponding author.
C. Gómez, J. Poza, and R. Hornero are with the Biomedical Engineering
Group at Department of Signal Theory and Communications, E.T.S.
Ingenieros de Telecomunicación, University of Valladolid, Campus Miguel
Delibes, 47011 – Valladolid, Spain (e-mail: cargom@tel.uva.es).
M. Martínez-Zarzuela and F. J. Díaz-Pernas are with the Industrial
Telematics Group, University of Valladolid, Spain.
A. Fernández is with the Centre for Biomedical Technology, Technical
University of Madrid, Spain.
978-1-4577-1787-1/12/$26.00 ©2012 IEEE 6188
depression should be attempted. The differential diagnosis
includes medical history studies, physical and neurological
evaluation, mental status tests, and neuroimaging techniques.
Nowadays, magnetoencephalography (MEG) recordings
are not used in AD clinical diagnosis, in spite of its potential
as aid diagnostic tool. MEG is a non-invasive technique that
records the electromagnetic fields produced by brain activity
with good temporal resolution. MEG technology offers some
advantages over electroencephalography (EEG). For
instance, magnetic fields are not distorted by the resistive
properties of the skull. Furthermore, EEG signals are
influenced by a wide variety of factors, such as distance
between sensors, electrode location, reference point or
conducting substance between skin and electrode. On the
other hand, the magnetic signals generated by the human
brain are extremely weak. Thus, SQUID (Superconducting
QUantum Interference Device) sensors are necessary to
detect them. In addition, MEG signals must be recorded in a
magnetically shielded room. Thus, MEG is characterized by
limited availability and high equipment cost.
Entropy is a concept addressing randomness and
predictability, with greater entropy often associated with
more randomness and less system order [3]. Mainly, there
are two families of entropy estimators: spectral entropies and
embedding entropies [4]. Spectral entropies extract
information from the amplitude component of the frequency
spectrum. On the other hand, embedding entropies are
calculated directly using the time series. This entropies
family provides information about how the signal fluctuates
with time by comparing the time series with a delayed
version of itself [4]. Both spectral and embedding entropies
have demonstrated their usefulness in the analysis of
EEG/MEG background activity in AD. An increase of
entropy values has been found using approximate entropy
(ApEn) [5], sample entropy [6], Shannon spectral entropy,
Rényi spectral entropy and Tsallis spectral entropy [7].
However, all these measures are applied to each EEG or
MEG channel independently. In the current study, we want
to go a step ahead, applying cross-approximate entropy
(Cross-ApEn) to MEG recordings from 12 AD patients and
12 age-matched control subjects. Cross-ApEn is a nonlinear
measure of asynchrony between time series. It has already
been used to study some biological signals, as hormone time
series dynamics [8], blood oxygen saturation and heart rate
[9].
The purpose of this study was to test the hypothesis that
Cross-ApEn values of the magnetic brain activity would be
different in both groups, hence indicating an abnormal type
of dynamics associated with AD.
II. MATERIALS AND METHODS
A. MEG recording
MEGs were recorded using a 148-channel whole-head
magnetometer (MAGNES 2500 WH, 4D Neuroimaging)
placed in a magnetically shielded room. The subjects lay on
a patient bed, in a relaxed state and with their eyes closed.
They were asked to stay awake and to avoid eye and head
movements. For each subject, five minutes of recording
were acquired at a sampling frequency of 678.17 Hz. These
recordings were down-sampled by a factor of four, obtaining
a sampling rate of 169.55 Hz. Data were digitally filtered
between 0.5 and 40 Hz. Finally, artifact-free epochs of 5
seconds (848 samples) were selected.
B. Subjects
The MEG data were acquired from 24 subjects. Twelve
patients (3 men and 9 women) fulfilling the criteria of
probable AD (age = 70.42 ± 9.04 years, mean ± standard
deviation SD) have participated in the present study. The
patients were diagnosed according to the criteria of the
National Institute of Communicative Disorders and Stroke
and the AD and Related Disorders Association (NINCDS-
ADRDA). The MMSE score was 17.00 ± 3.98 (Mean ± SD).
None of the patients used any kind of medication that could
have an influence on the MEG.
MEGs were also obtained from 12 age-matched control
subjects (5 men and 7 women, age = 70.42 ± 7.75 years,
MMSE = 29.50 ± 0.52, mean ± SD). The local ethics
committee approved the study. All control subjects and all
caregivers of the demented patients gave their informed
consent for the participation in the current research.
C. Cross Approximate Entropy (Cross-ApEn)
Cross-ApEn is a two-parameter family of statistics
introduced as a measure of asynchrony between two paired
time series [10]. It evaluates secondary as well as dominant
patterns in data, quantifying changes in underlying episodic
behavior that do no reflect in peak occurrences and
amplitudes [8]. To compute Cross-ApEn, two input
parameters must be specified: a run length m and a tolerance
window r. For two time series, u(i) and v(i), Cross-ApEn
measures, within tolerance r, the (conditional) regularity or
frequency of v-patterns similar to a given u-pattern of
window length m. Although m and r are critical in the
calculation of ApEn and Cross-ApEn, no guidelines exist to
optimize their values. However, values of m equal to 1 or 2,
and r between 0.1 and 0.25 has been suggested [10]. In this
pilot study, we have chosen m = 1 and r = 0.2 to compute
Cross-ApEn.
Given two equally sampled sequences of length N, u =
[u(1), u(2),…, u(N)] and v = [v(1), v(2),…, v(N)], the
6189
algorithm to compute Cross-ApEn is the following [9, 10]:
1) Normalize u(i) and v(i). The normalized time series u*(i)
and v*(i) are:
u * (i) = [ u(i) " mean(u)] /SD(u) (1)
v * (i) = [ v(i) " mean(v)] /SD(v) (2)
2) Form the vector sequences x(i) = [u*(i), u*(i+1),…,
u*(i+m–1)] and y(j) = [v*(j), v*(j+1),…, v*(j+m–1)].
These vectors represent m consecutive u* and v* values
starting with the ith and jth point, respectively.
3) Define the distance between x(i) and y(j), d[x(i), y(j)], as
the maximum absolute difference of their corresponding
scalar components:
d[ x(i), y( j)] = max u(i + k " 1) " v( j + k " 1) (3)
k=1,2,...,m
4) For each x(i), count the number of j (j=1,2,…,N!m+1)
so that d[x(i), y(j)]!r, denoted as Nim(r). Then, for
i=1,2,…,N!m+1, set
N im (r)
C im (r)(v u) = (4)
N " m +1
5) Compute the natural logarithm of each Cim(r) and
average it over i:
N #m+1
1
" m (r)(v u) = $ lnC im (r)(v u)
N # m + 1 i=1
(5)
6) Finally, Cross-ApEn is defined by:
Cross - ApEn(m, r,N )(v u) = " m (r)(v u) # " m+1 (r)(v u) (6)
It is important to note that Cross-ApEn is not always
defined because Cim(r)(v||u) may be equal to 0 in the absence
of similar patterns between u and v. To solve this, two
correction strategies have been proposed [11]: bias 0 and
bias max. In this study, both correction strategies have been
applied. Both strategies assign non zero values to Cim(r)(v||u)
and Cim+1(r)(v||u) in the absence of matches, as follows:
1) Bias 0: Cim(r) = Cim+1(r) = 1 if originally Cim(r) =
Cim+1(r) = 0, and Cim+1(r) = (N–m)–1 if originally Cim(r) "
0 and Cim+1(r) = 0.
2) Bias max: Cim(r) = 1 if originally Cim(r) = 0, and Cim+1(r)
= (N–m+1)–1 if originally Cim+1(r) = 0.
III. RESULTS
Cross-ApEn algorithm was applied to the MEG
recordings with parameter values of m = 1 and r = 0.2 and
both correction strategies bias 0 and biax max. The end
result of computing Cross-ApEn for all pair-wise
combinations of MEG channels is a B ! B matrix with B =
148 (number of channels), where each entry Bi,j contains the
Cross-ApEn value for channels i and j. It is important to note
that there is a direction dependence, due to the fact that
"m(r)(v||u) will note generally be equal to "m(r)(u||v). This
may be considered an advantage over other synchrony
methods as coherence or synchronization likelihood. Fig. 1
and 2 summarize the average Cross-ApEn values estimated
at both groups for all the pair-wise combinations of MEG
channels using bias 0 and bias max corrections, respectively.
This figures show that entropy values were lower in the AD
group than in the control group for all channels
combinations, which suggests that this disorder is
accompanied by a MEG asynchrony decrease. Differences
between patients and controls were statistically significant
(Student’s t-test) in 55.69% of the 148 ! 148 MEG
combinations using bias 0 correction, and in 63.66% using
bias max correction. As a multiple comparison correction
has not been performed, these results should be taken with
caution.
Furthermore, we evaluated the ability of Cross-ApEn to
discriminate AD patients from elderly control subjects by
means of receiver operating characteristic (ROC) curves. A
ROC curve is a graphical representation of the trade-offs
between sensitivity and specificity. We define sensitivity as
the rate of ADHD patients who test positive, whereas
specificity represents the fraction of controls correctly
recognized. Accuracy quantifies the total number of subjects
precisely classified. The area under the ROC curve (AROC)
is a single number summarizing the performance. AROC
indicates the probability that a randomly selected AD patient
has a Cross-ApEn value lower than a randomly chosen
control subject. In order to calculate these values, a leave-
one-out cross-validation procedure was used. In the leave-
one-out method, the data from one subject are excluded from
the training set one at a time and then classified on the basis
of the threshold calculated from the data of all other
subjects. The leave-one-out cross-validation procedure
provides a nearly unbiased estimate of the true error rate of
the classification procedure. To simplify the analyses, we
calculate the mean value of all the 148 ! 148 Cross-ApEn
values, for bias 0 and bias max corrections. For both
Control group
Fig. 1. Average Cross-ApEn values with bias 0 correction for AD and control groups.
6190
correction strategies, we obtained the same accuracy
(70.83%), sensitivity (66.67%), specificity (75.00%) and
AROC (0.83) values.
IV. DISCUSSION AND CONCLUSIONS
We analyzed the MEG background activity from 12 AD
patients and 12 control subjects by means of Cross-ApEn.
Our purpose was to test the hypothesis that the brain activity
recorded in MEG signals can reflect a disconnection
syndrome in AD patients.
Cross-ApEn has proven to be effective in discriminating
AD patients from controls. Our study revealed that AD
subjects have lower connectivity/asynchrony values. Our
findings support the notion that AD involves a loss of
functional connectivity. Moreover, significant statistical
differences were found in several combinations of MEG
channels. However, these findings are preliminary and
require replication in a larger patient population before any
conclusion can be made about the clinical diagnostic value
of this measure.
Several studies have shown the loss of brain connectivity
in AD using EEG and MEG recordings. Most of these
studies were carried out using the well-known coherence
[12]. The main finding is a lower synchronization level in
alpha and beta frequency bands. Nevertheless, contradictory
results have been found in the other frequency bands [2].
More recently, other connectivity methods have been used to
analyze the brain activity in AD, as cross mutual information
[13], global field synchronization [14], and synchronization
likelihood [15]. For instance, Jeong et al. [13] found that
cross mutual information in EEGs from AD patients was
lower than in normal controls, especially over frontal and
Alzheimer’s disease group
antero-temporal brain regions. Using global field
synchronization, similar results were found: patients showed
decreased synchronization values in almost all frequency
bands [14]. These results may confirm the hypothesized
disconnection syndrome. This connectivity loss in AD may
be due to the fact that neuritic plaques appears organized in
AD patients’ brains, affecting the ends of corticocortical
connections [16].
ROC curves were used to assess the ability of Cross-ApEn
to classify ADHD patients and control subjects. We reached
an accuracy of 70.83% (66.67% sensitivity, 75% specificity)
and a value of area under the ROC curve of 0.83.
Nevertheless, these values should be taken with caution due
to the small sample size.
In sum, our study leads us to conclude that MEG
background activity in AD patients is accompanied by a
brain asynchrony decrease. The results obtained with Cross-
ApEn showed significant differences between AD patients
and controls, indicating an abnormal type of dynamics
associated with this disorder.
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Alzheimer’s disease group
Goldschmidtboeing, Frank ................................................................................................................ WeB07.3 .............. 535
Goldstein, Goldie ............................................................................................................................... ThC04.3 ............. 3163
Goletsis, Yorgos ................................................................................................................................ WeC13.1 ............ 1262
.......................................................................................................................................................... WeD26.4 ............ 2206
Gollmer, Sebastian T. ....................................................................................................................... FrA05.5 .............. 3990
Golub, Matthew D. ............................................................................................................................ WeC15.5 ............ 1327
Golzan, S.Mojtaba ............................................................................................................................. ThD01.5 ............. 3384
.......................................................................................................................................................... FrD03.12 ............ 5278
Gomes, Pedro Tiago ......................................................................................................................... WeD24.4 ............ 2128
.......................................................................................................................................................... SaC14.4 ............. 6695
Gomez Tames, Jose David ............................................................................................................... ThD06.6 ............. 3576
Gomez, Carlos .................................................................................................................................. ThD02.10 ........... 3444
.......................................................................................................................................................... SaA02.4 ............. 6188
Gomez, James .................................................................................................................................. SaC14.1 ............. 6681
Gómez, Juan ..................................................................................................................................... WeE16.3 ............ 2522
Gomez-Clapers, Joan ....................................................................................................................... WeB08.1 .............. 550
.......................................................................................................................................................... FrC09.2 .............. 5034
Gomez-Foix, Anna Mª ....................................................................................................................... WeE18.3 ............ 2571
Gómez-García, Jorge Andrés ........................................................................................................... FrB01.9 .............. 4217
Gomis Gascó, Sergi .......................................................................................................................... WeA13.2 .............. 248
.......................................................................................................................................................... FrC14.5 .............. 5118
Gonçalves da Silva, Chagas, Vitoria ................................................................................................. WeD07.3 ............ 1578
Goncalves, Carlos Alberto ................................................................................................................ ThD06.10 ........... 3592
Gonenc, Berk .................................................................................................................................... WeC19.1 ............ 1401
Gong, Enhao ..................................................................................................................................... ThC15.6 ............. 3292
Gonzalez, Alejandro .......................................................................................................................... FrB20.8 .............. 4843
Gonzalez, Jose ................................................................................................................................. WeD13.2 ............ 1789
.......................................................................................................................................................... ThD06.6 ............. 3576
.......................................................................................................................................................... FrB05.1 .............. 4345
González-Arriaga, Oscar Hugo ......................................................................................................... FrB03.6 .............. 4262
Gonzalez-Camarena, Ramon ........................................................................................................... WeB11.1 .............. 605
Gonzalez-Martinez, Jorge ................................................................................................................. FrC17.3 .............. 5158
González-Suárez, Juan Manuel ........................................................................................................ WeC07.4 ............ 1165
Good, Norm ....................................................................................................................................... FrD24.9 .............. 5903
Goodwin, Antony ............................................................................................................................... FrB16.9 .............. 4631
Goodwin, Matthew ............................................................................................................................ FrA08.3 .............. 4046
Gopalakrishna, Vanishree ................................................................................................................. WeE03.5 ............ 2271
Gopinath, Ajay ................................................................................................................................... FrA06.3 .............. 4006
Gorbet, Rob ....................................................................................................................................... SaC19.1 ............. 6780
Gorgian Mohammadi, Amrollah ........................................................................................................ FrB04.4 .............. 4303
Górriz-Sáez, Juan Manuel ................................................................................................................ SaA06.4 ............. 6255
Goska, Benjamin ............................................................................................................................... WeD20.7 ............ 2017
Gosselin, Benoit ................................................................................................................................ WeD10.1 ............ 1659
.......................................................................................................................................................... FrE08.6 .............. 6015
Gott, Shannon ................................................................................................................................... WeD09.3 ............ 1639
.......................................................................................................................................................... FrD17.3 .............. 5666
Gottshall, Kim .................................................................................................................................... FrE17.4 .............. 6141
Goubran, Rafik A. .............................................................................................................................. WeA14.2 .............. 268
.......................................................................................................................................................... FrD22.3 .............. 5810
Goudas, Theodosis ........................................................................................................................... FrB08.6 .............. 4414
.......................................................................................................................................................... FrB08.7 .............. 4418
Goudey, Benjamin ............................................................................................................................. WeC11.6 ............ 1258
Goulding, Evan .................................................................................................................................. WeE08.5 ............ 2392