Alterations in Memory Networks in Mild Cognitive Impairment and Alzheimer's Disease: An Independent Component Analysis

By K. Celone, Vince D. Calhoun, Bradford C. Dickerson, Alireza Atri, E. Chua, Saul L. Miller, Kristina Depeau, D. Rentz, D. Selkoe, Deborah Blacker and 2 more. Journal of Neuroscience, 2006

750 citations recorded by the source corpus.

Memory function is likely subserved by multiple distributed neural networks, which are disrupted by the pathophysiological process of Alzheimer's disease (AD). In this study, we used multivariate analytic techniques to investigate memory-related functional magnetic resonance imaging (fMRI) activity in 52 individuals across the continuum of normal aging, mild cognitive impairment (MCI), and mild AD. Independent component analyses revealed specific memory-related networks that activated or deactivated during an associative memory paradigm. Across all subjects, hippocampal activation and parietal deactivation demonstrated a strong reciprocal relationship. Furthermore, we found evidence of a nonlinear trajectory of fMRI activation across the continuum of impairment. Less impaired MCI subjects showed paradoxical hyperactivation in the hippocampus compared with controls, whereas more impaired MCI subjects demonstrated significant hypoactivation, similar to the levels observed in the mild AD subjects. We found a remarkably parallel curve in the pattern of memory-related deactivation in medial and lateral parietal regions with greater deactivation in less-impaired MCI and loss of deactivation in more impaired MCI and mild AD subjects. Interestingly, the failure of deactivation in these regions was also associated with increased positive activity in a neocortical attentional network in MCI and AD. Our findings suggest that loss of functional integrity of the hippocampal-based memory systems is directly related to alterations of neural activity in parietal regions seen over the course of MCI and AD. These data may also provide functional evidence of the interaction between neocortical and medial temporal lobe pathology in early AD.

Subfields: Cognitive Neuroscience, Psychiatry and Mental health, Radiology, Nuclear Medicine and Imaging

View Paper: https://www.semanticscholar.org/paper/9f1736afd652e7b72c02526fc3ffe888d92292eb

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Citations in the corpus

Network Analysis of Intrinsic Functional Brain Connectivity in Alzheimer's Disease (2008, background): “Three recent studies have reported reduced default-mode network deactivation in MCI and/ or AD patients during encoding tasks [12,13] and during a semantic classification task [14].”
The Brain's Default Network (2008, methodology): “…network have been explored in AD using both analysis of task-induced deactivation (Lustig 2003, see also Greicius et al. 2004). et al. 2003, Celone et al. 2006) and analysis of intrinsic activity correlations (Greicius et al. 2004, Rombouts et al. 2005, Celone et al. 2006, Wang et al. 2006).”
The Cortical Signature of Alzheimer's Disease: Regionally Specific Cortical Thinning Relates to Symptom Severity in Very Mild to Mild AD Dementia and is Detectable in Asymptomatic Amyloid-Positive Individuals (2008, background): “…that described above (details have been previously published as cited below), with 39 participants in Sample 2 (Atri et al. 2005), 41 participants in Sample 3 (Wright, Dickerson, et al. 2007; Wright, Feczko, et al. 2007), and 40 participants in Sample 4 (Dickerson et al. 2005; Celone et al. 2006).”
Brain imaging in Alzheimer disease. (2012, background): “of MCI, followed by a loss of activation in late stages of MCI, similar to the pattern seen in AD patients (Celone et al. 2006).”
Reduction of hippocampal hyperactivity improves cognition in amnestic mild cognitive impairment (2012, result): “Contrary to the view that greater hippocampal activationmight serve a beneficial function, these results support the view that increased hippocampal activation in aMCI is a dysfunctional condition and that targeting excess hippocampal activity has therapeutic potential.”
Que PASA? The posterior-anterior shift in aging. (2008, background): “…with deactivations in posterior midline cortex (Daselaar et al. 2004), and failure to deactivate this region has been associated with memory deﬁcits in healthy aging and Alzheimer’s disease (Daselaar et al. 2003; Lustig et al. 2003; Greicius et al. 2004; Celone et al. 2006; Grady et al. 2006).”
State-space model with deep learning for functional dynamics estimation in resting-state fMRI (2016, positive): “This can be linked with the previous studies (Grady et al., 2003; Celone et al., 2006; Bai et al., 2009; Das et al., 2013) that suggested the compensation of the cognitive functional losses caused by pathologies of brain disorder.”
A review of group ICA for fMRI data and ICA for joint inference of imaging, genetic, and ERP data (2008, neutral): “An in-between approach would be to utilize temporal concatenation separately for each group (Celone et al., 2006), although in this case matching the components post hoc becomes again necessary.”
Identification of MCI Individuals Using Structural and Functional Connectivity Networks (2011, result): “The regions selected in the course of classification by our method are in agreement with previous studies and include the prefrontal cortex and or-bitofrontal cortex [14], temporal pole [13], anterior and posterior cingulate gyrus, precuneus and insula [8], amygdala [7], thalamus [30], parahippocamp”
Multi-subject Independent Component Analysis of fMRI: A Decade of Intrinsic Networks, Default Mode, and Neurodiagnostic Discovery (2012, neutral): “Early work focused on schizophrenia [10], [64], substance use [7], and Alzheimer’s disease [11], and mild cognitive impairment [50], [78].”
High-resolution structural and functional MRI of hippocampal CA3 and dentate gyrus in patients with amnestic mild cognitive impairment (2010, background): “Previous studies of MCI patients have noted elevated BOLD fMRI signals in the hippocampus and parahippocampal gyrus during a variety of memory tasks (Celone et al., 2006; Dickerson et al., 2005; Hamalainen et al., 2007; Johnson et al., 2006), as noted above, although none of the studies localized th”
Comparison of multi-subject ICA methods for analysis of fMRI data (2010, methodology): “An intermediate approach would use temporal concatenation separately for each group [Celone et al., 2006], although in this case, matching the components post hoc becomes again necessary.”
Structural Insights into Aberrant Topological Patterns of Large-Scale Cortical Networks in Alzheimer's Disease (2008, background): “, 2001, 2003), hippocampus (Celone et al., 2006; Wang et al., 2006), cingulate (Greicius et al.”