Resting Brain Connectivity: Changes during the Progress of Alzheimer Disease

Zhang, Hongying; Wang, Shijie; Liu, Bin; Ma, Zhanlong; Yang, Ming; Zhang, Zhijun; Teng, Gao‐Jun

doi:10.1148/radiol.10091701

Cited by 280 publications

(229 citation statements)

References 33 publications

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“…48 Similarly, increased resting-state connectivity between the PCC and other DMN regions has been noted in elderly individuals with elevated regional brain atrophy and memory complaints, 91 in MCI, 47,92,93 and in the very early stages of AD. 85,94,95 The concordance between the current results and those in neurodegenerative disease orients us to the potential consequences of TBIinduced network changes on long-term neurological status. Wholebrain functional connectivity analyses, naïve of any seed definitions, have suggested that individuals advance toward a more ''healthy'' state in the months after injury, 13 corresponding to significant clinical recovery in the first year.…”

Section: Potential Markers Of Long-term Outcomesupporting

confidence: 69%

“…For example, it has been found that restingstate antiphase synchrony between regions of different networks is impaired in AD, 48,[83][84][85] and the loss of antiphase synchrony between posterior regions and frontal cortex in AD-risk populations may be especially relevant to the development of AD. 47 Hippocampal hypersynchrony with proximal regions and/or other regions of the DMN has been noted in risk groups for AD, including individuals positive for the apolipoprotein Ee4 allele [86][87][88] and mild cognitive impairment (MCI) patients 89,90 as well as individuals with early AD itself.…”

Section: Potential Markers Of Long-term Outcomementioning

confidence: 99%

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Chronology and Chronicity of Altered Resting-State Functional Connectivity after Traumatic Brain Injury

Venkatesan

Dennis

Hillary

2015

Journal of Neurotrauma

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Whereas traumatic brain injury (TBI) results in widespread disruption of neural networks, changes in regional resting-state functional connectivity patterns after insult remain unclear. Specifically, little is known about the chronology of emergent connectivity alterations and whether they persist after a critical recovery window. We used resting-state functional magnetic resonance imaging and seed-voxel correlational analyses in both cross-sectional and longitudinal designs to probe intrinsic connectivity patterns involving the posterior cingulate cortex (PCC) and hippocampi, regions shown to be important in the default mode network (DMN) and vulnerable to neuropathology. A total of 22 participants in the chronic stage of moderateto-severe TBI and 18 healthy controls were included for cross-sectional study. Longitudinal analyses included 13 individuals in the TBI group for whom data approximately 3 months after injury (subacute) were available. Overall, results indicated dissociable connectivity trajectories of the PCC and hippocampi during recovery from TBI, with PCC alterations characterized by early hypersynchrony with the anterior DMN that is gradually reduced, and hippocampal changes marked by increasing synchrony with proximal cortex and subcortex. The PCC also showed increasing antiphase synchrony with posterior attentional regions, and the hippocampi showed decreasing antiphase synchrony with frontal attentional regions. Antiphase synchrony of the hippocampus and dorsolateral prefrontal cortex at the subacute stage of TBI was positively associated with attentional performance on neuropsychological tests at both the subacute and chronic stages. Our findings highlight the heterogeneity of regional whole-brain connectivity changes after TBI, and suggest that residual connectivity alterations exist in the clinically stable phase of TBI. Parallels between the chronicity of the observed effects and findings in neurodegenerative disease are discussed in the context of potential long-term outcomes of TBI.

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Section: Potential Markers Of Long-term Outcomesupporting

confidence: 69%

Section: Potential Markers Of Long-term Outcomementioning

confidence: 99%

Chronology and Chronicity of Altered Resting-State Functional Connectivity after Traumatic Brain Injury

Venkatesan

Dennis

Hillary

2015

Journal of Neurotrauma

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“…Analyses of AD‐related functional brain network differences associated with the DMN but not part of the DMN report changes in superior parietal and occipital regions (Agosta et al., 2012; Lee et al., 2016). These findings are consistent with those in resting and visual fMRI studies that report affected visual functioning accompanied by differences in the visual cortices (Alegret et al., 2010; Lehmann et al., 2013; Wang et al., 2015; Zhang et al., 2010) and the idea that deviations from the typical pathology, such as the involvement of functionally specific brain regions, drive the variation in neurodegenerative variation in AD.…”

Section: Discussionmentioning

confidence: 99%

Functional brain network centrality is related to APOE genotype in cognitively normal elderly

et al. 2018

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IntroductionAmyloid plaque deposition in the brain is an early pathological change in Alzheimer's disease (AD), causing disrupted synaptic connections. Brain network disruptions in AD have been demonstrated with eigenvector centrality (EC), a measure that identifies central regions within networks. Carrying an apolipoprotein (APOE)‐ε4 allele is a genetic risk for AD, associated with increased amyloid deposition. We studied whether APOE‐ε4 carriership is associated with EC disruptions in cognitively normal individuals.MethodsA total of 261 healthy middle‐aged to older adults (mean age 56.6 years) were divided into high‐risk (APOE‐ε4 carriers) and low‐risk (noncarriers) groups. EC was computed from resting‐state functional MRI data. Clusters of between‐group differences were assessed with a permutation‐based method. Correlations between cluster mean EC with brain volume, CSF biomarkers, and psychological test scores were assessed.ResultsDecreased EC in the visual cortex was associated with APOE‐ε4 carriership, a genetic risk factor for AD. EC differences were correlated with age, CSF amyloid levels, and scores on the trail‐making and 15‐object recognition tests.ConclusionOur findings suggest that the APOE‐ε4 genotype affects brain connectivity in regions previously found to be abnormal in AD as a sign of very early disease‐related pathology. These differences were too subtle in healthy elderly to use EC for single‐subject prediction of APOE genotype.

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“…The DMN is typically found deactivated during cognitive tasks requiring externally focused attention and activated during internally focused mental tasks, such as episodic memory retrieval, mental state attribution, and visual imagery (Buckner, Andrews-Hanna, & Schacter, 2008;Mason et al, 2007;Raichle et al, 2001;Shulman et al, 1997). In addition to the regional atrophy and neuronal hypometabolism affecting DMN nodes, disruptions in functional connectivity of the DMN in AD dementia have been widely replicated (Agosta et al, 2012;Binnewijzend et al, 2012;Greicius, Srivastava, Reiss, & Menon, 2004), and have been linked to core memory and visuospatial deficits Supekar, Menon, Rubin, Musen, & Greicius, 2008;Zhang et al, 2010). Intriguingly, connectivity disruption and impaired task-related down regulation of the DMN may already emerge during the presymptomatic phase of AD as modeled cross-sectionally on the basis of imaging evidence of cortical amyloid pathology Sperling et al, 2009) or an apolipoprotein E4 (APOE4) positive genotype, which is a major genetic risk factor for late onset AD (Damoiseaux et al, 2012;Machulda et al, 2011;Persson et al, 2008).…”

Section: Functional Connectivity Changes In the Course Of Admentioning

confidence: 99%

Measuring Cortical Connectivity in Alzheimer’s Disease as a Brain Neural Network Pathology: Toward Clinical Applications

Teipel

Grothe

Zhou

et al. 2016

J Int Neuropsychol Soc

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Objectives: The objective was to review the literature on diffusion tensor imaging as well as resting-state functional magnetic resonance imaging and electroencephalography (EEG) to unveil neuroanatomical and neurophysiological substrates of Alzheimer's disease (AD) as a brain neural network pathology affecting structural and functional cortical connectivity underlying human cognition. Methods: We reviewed papers registered in PubMed and other scientific repositories on the use of these techniques in amnesic mild cognitive impairment (MCI) and clinically mild AD dementia patients compared to cognitively intact elderly individuals (Controls). Results: Hundreds of peer-reviewed (cross-sectional and longitudinal) papers have shown in patients with MCI and mild AD compared to Controls (1) impairment of callosal (splenium), thalamic, and anterior-posterior white matter bundles; (2) reduced correlation of resting state blood oxygen level-dependent activity across several intrinsic brain circuits including default mode and attention-related networks; and (3) abnormal power and functional coupling of resting state cortical EEG rhythms. Clinical applications of these measures are still limited. Conclusions: Structural and functional (in vivo) cortical connectivity measures represent a reliable marker of cerebral reserve capacity and should be used to predict and monitor the evolution of AD and its relative impact on cognitive domains in pre-clinical, prodromal, and dementia stages of AD. (JINS, 2016, 22, 138-163)

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Resting Brain Connectivity: Changes during the Progress of Alzheimer Disease

Cited by 280 publications

References 33 publications

Chronology and Chronicity of Altered Resting-State Functional Connectivity after Traumatic Brain Injury

Chronology and Chronicity of Altered Resting-State Functional Connectivity after Traumatic Brain Injury

Functional brain network centrality is related to APOE genotype in cognitively normal elderly

Measuring Cortical Connectivity in Alzheimer’s Disease as a Brain Neural Network Pathology: Toward Clinical Applications

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