Kun Yue1, Jason M Webster2, Thomas J Grabowski2, Ali Shojaei1, and Hesamoddin Jahanian2
1Department of Biostatistics, University of Washington, Seattle, WA, United States, 2Department of Radiology, University of Washington, Seattle, WA, United States
Synopsis
With
advances in experimental therapeutics for Alzheimer's Disease (AD) the need for an accurate,
non-invasive and widely available AD biomarker is more pressing than ever. Resting-state
functional connectivity in default mode network is a candidate biomarker that
is gaining traction in the field. However, the traditional stationary
measurement of the default mode network connectivity cannot capture complicated dynamic patterns of functional connectivity that exist in the brain. Here, we have proposed a novel, reliable
technique, based on Dynamic
Condtional Correlation model, to quantify the dynamic functional connectivity in the brain and evaluated its sensitivity to cerebrospinal
fluid biomarkers in AD.
Introduction
To be able to apply treatments in
earlier stages of Alzheimer’s disease (AD), there is a need for non-invasive
and widely available biomarkers that can identify the initiation of the disease
(i.e. Aβ positivity) even while clinical symptoms are not yet
present. Such a biomarker would provide the opportunity to stop or delay the
disease progression before irreversible damage has been done. Many studies have
reported alteration in intrinsic functional connectivity of the
default mode network (DMN) in AD. However, the diagnosis accuracy of these measurements has not been sufficient for a useful biomarker in AD [1]. We hypothesize that it is partly due to the fact that most of
these studies have focused on the stationary measures of functional connectivity, which ignores the complicated dynamic patterns of
network configuration that exist in the brain. To address
this shortcoming, here we propose a novel, reliable technique to quantify
dynamic functional connectivity in the DMN that is sensitive to the subject’s cerebrospinal
fluid (CSF) Aβ biomarkers of AD.Methods
Data: 87 subjects (mean age= 74 yr, range = 54-91 yr) were recruited for this study. CSF was collected from all subjects via lumbar puncture and processed on a Millipore Milliplex MAP Human Aβ Panel. Subjects included 66 cognitively normal (38 women), 16 mild cognitive impairment (7 women), and 5 AD dementia (3 women) patients. We scanned all subjects on a 3T (Philips Achieva) scanner using a 32-channel head coil. Resting
state fMRI (rs-fMRI) data was collected using a 2D Multi Echo EPI sequence (3.5 mm isotropic voxels, TR/TEs = 2,500/9.5, 27.5, 45.5 ms). Each rs-fMRI run acquired 240 time points
of data (10 min). A structural T1-weighted 3D MPRAGE with 0.8 mm isotropic voxels was also obtained for co-registration. rs-fMRI data was preprocessed using TEDANA [2], motion corrected and spatially normalized to MNI space. In this study, we
focused on the following DMN nodes: posterior cingulate cortex, medial prefrontal cortex, left and right angular gyrus, left and right dorsal medial prefrontal cortex, and left and right parahippocampal cortex. We created a mask for each of these nodes
using a standard group-level ICA analysis performed across all subjects. Using these
masks, the corresponding time-series were extracted for each node. Each
time-series was pre-whitened using a data-driven ARMA model. For each
times-series, the ARMA order was determined based on the Bayesian information
criteria (BIC) [3]. We fit the ARMA model to each time-series separately and keep
the residuals from this model as the pre-whitened data. The dynamic functional
connectivity was then quantified using the Dynamic Condtional Correlation
(DCC)-GARCH Model (Figure 1).
DCC-GARCH model: is a
flexible tool to model the temporal variation in the second moment of a
multivariate time-series [4]. More specifically, DCC-GARCH model allows the
correlation matrix to depend on time and describe a plausible mechanism for the
temporal variation of the correlation matrix. The two major parameters of the
model (referred to as α and β in this abstract) provide a straightforward
representation of how fast the correlations variate, and how volatile the
correlations can be. α represents how the correlation matrix show dynamic
variations as a response to new stimulates, and β represents how stable the
correlation matrix is over time. The simulation presented in Figure 2, shows
how these parameters represent different correlational structures of dynamic time-series
data (Figure 2).Results
We
inspected the distribution of the observations to choose the distributional
assumption in the DCC model (Figure 3) and used normal distribution assumption
for the error terms when fitting the DCC model. For each subject we quantified
the dynamic functional connectivity of DMN using the DCC model and
calculated the α and β parameters. We divided the subjects into two group based on their CSF Aβ42/40
ratio which is the most accurate CSF biomarker for Aβ positivity in clinical AD
[5]. The internally determined [6] cut-off threshold of 0.11 was used for dividing
subjects into Aβ+ (AD) and Aβ- (control) groups. p-value of two sample t-test was then
calculated for evaluating the group difference in α and β parameter
estimates. For comparison, we also measured the mean stationary measure of DMN connectivity for each subject using the dual regression ICA method [7] (Figure 4).Discussion
In
this study we proposed a novel method based on the DCC-GARCH model to quantify dynamic functional
connectivity. We used the proposed method to
quantify the dynamic functional connectivity in the DMN and
investigated its sensitivity to Aβ status of the subjects, determined by their CSF Aβ measurements.
Unlike conventional stationary measures of the DMN
functional connectivity, the proposed method was sensitive to the CSF Aβ status of the subjects. Our results show that AD patients (i.e. Aβ+ subjects) have lower α and higher β values (i.e. less dynamic and more invariant connectivity in the DMN over time) compared with controls (Aβ- subjects). These preliminary findings need to be confirmed in larger cohorts.Conclusion
This study suggests that dynamic functional connectivity in the DMN, quantified using the proposed method, may provide a sensitive, non-invasive biomarker to differentiate between Aβ+ and Aβ- subjects and improve our ability to detect and apply treatments in
earlier stages of AD.Acknowledgements
This work is supported by the University of Washington Alzheimer’s Disease Research center pilot project award, Weill Neurohub, and NIH grants P50 AG047366 and 1K01AG071798-01.References
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