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Richness in Functional Connectivity Depends on the Neuronal Integrity within the Posterior Cingulate Cortex.

ABSTRACT: The brain's connectivity skeleton-a rich club of strongly interconnected members-was initially shown to exist in human structural networks, but recent evidence suggests a functional counterpart. This rich club typically includes key regions (or hubs) from multiple canonical networks, reducing the cost of inter-network communication. The posterior cingulate cortex (PCC), a hub node embedded within the default mode network, is known to facilitate communication between brain networks and is a key member of the "rich club." Here, we assessed how metabolic signatures of neuronal integrity and cortical thickness influence the global extent of a functional rich club as measured using the functional rich club coefficient (fRCC). Rich club estimation was performed on functional connectivity of resting state brain signals acquired at 3T in 48 healthy adult subjects. Magnetic resonance spectroscopy was measured in the same session using a point resolved spectroscopy sequence. We confirmed convergence of functional rich club with a previously established structural rich club. N-acetyl aspartate (NAA) in the PCC is significantly correlated with age (p = 0.001), while the rich club coefficient showed no effect of age (p = 0.106). In addition, we found a significant quadratic relationship between fRCC and NAA concentration in PCC (p = 0.009). Furthermore, cortical thinning in the PCC was correlated with a reduced rich club coefficient after accounting for age and NAA. In conclusion, we found that the fRCC is related to a marker of neuronal integrity in a key region of the cingulate cortex. Furthermore, cortical thinning in the same area was observed, suggesting that both cortical thinning and neuronal integrity in the hub regions influence functional integration of at a whole brain level.

SUBMITTER: Lord AR

PROVIDER: S-EPMC5384321 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature

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Richness in Functional Connectivity Depends on the Neuronal Integrity within the Posterior Cingulate Cortex.

Lord Anton R AR Li Meng M Demenescu Liliana R LR van den Meer Johan J Borchardt Viola V Krause Anna Linda AL Heinze Hans-Jochen HJ Breakspear Michael M Walter Martin M

Frontiers in neuroscience 20170407

The brain's connectivity skeleton-a rich club of strongly interconnected members-was initially shown to exist in human structural networks, but recent evidence suggests a functional counterpart. This rich club typically includes key regions (or hubs) from multiple canonical networks, reducing the cost of inter-network communication. The posterior cingulate cortex (PCC), a hub node embedded within the default mode network, is known to facilitate communication between brain networks and is a key m ...[more]

PMID: 28439224

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Project description:ObjectiveWe aimed to investigate the alterations of brain functional connectivity (FC) in type 2 diabetes mellitus (T2DM) patients without clinical evidence of cognitive impairment and microvascular complications (woCIMC-T2DM) using resting-state functional MRI (rs-fMRI) and to determine whether its value was correlated with clinical indicators.MethodsA total of 27 T2DM and 26 healthy controls (HCs) were prospectively examined. Cognitive impairment was excluded using the Mini-Mental State Examination (MMSE) and the Montreal Cognitive Assessment (MoCA) scales, and microvascular complications were excluded by fundus photography, microalbuminuria, and other indicators. The correlation maps, derived from rs-fMRI with posterior cingulate cortex (PCC) as the seed, were compared between T2DM patients and HCs. Pearson's correlation analysis was performed to determine the relationship between the FC of PCC and the clinical indicators.ResultsCompared with HC, woCIMC-T2DM patients showed significantly decreased FCs with PCC (PCC-FCs) in the anterior cingulate cortex (ACC), right superior frontal gyrus, right medial frontal gyrus, and right angular gyrus. Meanwhile, increased PCC-FCs was observed in the right superior temporal gyrus and calcarine fissure (CAL). The FC of PCC-ACC was negatively correlated with glycosylated hemoglobin (HbA1c) and diabetes duration, and the FC of PCC-CAL was significantly positively correlated with HbA1c and diabetes duration.ConclusionThe FC, especially of the PCC with cognitive and visual brain regions, was altered before clinically measurable cognitive impairment and microvascular complications occurred in T2DM patients. In addition, the FC of the PCC with cognitive and visual brain regions was correlated with HbA1c and diabetes duration. This indicates that clinicians should pay attention not only to blood glucose control but also to brain function changes before the occurrence of adverse complications, which is of great significance for the prevention of cognitive dysfunction and visual impairment.

Project description:The posterior cingulate cortex (PCC) is a critical brain network hub particularly sensitive to Alzheimer's disease (AD) and can be subdivided into ventral (vPCC) and dorsal (dPCC) regions. The aim of the present study was to highlight functional connectivity (FC) disruption, atrophy, and hypometabolism within the ventral and dorsal PCC networks in patients with amnestic mild cognitive impairment (aMCI) or AD. Forty-three healthy elders (HE) (68.7 ± 6 years), 34 aMCI (73.4 ± 6.8 years) and 24 AD (70.9 ± 9.1 years) patients underwent resting-state functional MRI, anatomical T1-weighted MRI and FDG-PET scans. We compared FC maps obtained from the vPCC and dPCC seeds in HE to identify the ventral and dorsal PCC networks. We then compared patients and HE on FC, gray matter volume and metabolism within each network. In HE, the ventral PCC network involved the hippocampus and posterior occipitotemporal and temporoparietal regions, whereas the dorsal PCC network included mainly frontal, middle temporal and temporoparietal areas. aMCI patients had impaired ventral network FC in the bilateral hippocampus, but dorsal network FC was preserved. In AD, the ventral network FC disruption had spread to the left parahippocampal and angular regions, while the dorsal network FC was also affected in the right middle temporal cortex. The ventral network was atrophied in the bilateral hippocampus in aMCI patients, and in the vPCC and angular regions as well in AD patients. The dorsal network was only atrophied in AD patients, in the dPCC, bilateral supramarginal and temporal regions. By contrast, hypometabolism was already present in both the vPCC and dPCC networks in aMCI patients, and further extended to include the whole networks in AD patients. The vPCC and dPCC connectivity networks were differentially sensitive to AD. Atrophy and FC disruption were only present in the vPCC network in aMCI patients, and extended to the dPCC network in AD patients, suggesting that the pathology spreads from the vPCC to the dPCC networks. By contrast, hypometabolism seemed to follow a different route, as it was present in both networks since the aMCI stage, possibly reflecting not only local disruption but also distant synaptic dysfunction.

Project description:The intrinsic connectivity of the default mode network has been associated with the level of consciousness in patients with severe brain injury. Especially medial parietal regions are considered to be highly involved in impaired consciousness. To better understand what aspect of this intrinsic architecture is linked to consciousness, we applied spectral dynamic causal modeling to assess effective connectivity within the default mode network in patients with disorders of consciousness. We included 12 controls, 12 patients in minimally conscious state and 13 in vegetative state in this study. For each subject, we first defined the four key regions of the default mode network employing a subject-specific independent component analysis approach. The resulting regions were then included as nodes in a spectral dynamic causal modeling analysis in order to assess how the causal interactions across these regions as well as the characteristics of neuronal fluctuations change with the level of consciousness. The resulting pattern of interaction in controls identified the posterior cingulate cortex as the main driven hub with positive afferent but negative efferent connections. In patients, this pattern appears to be disrupted. Moreover, the vegetative state patients exhibit significantly reduced self-inhibition and increased oscillations in the posterior cingulate cortex compared to minimally conscious state and controls. Finally, the degree of self-inhibition and strength of oscillation in this region is correlated with the level of consciousness. These findings indicate that the equilibrium between excitatory connectivity towards posterior cingulate cortex and its feedback projections is a key aspect of the relationship between alterations in consciousness after severe brain injury and the intrinsic functional architecture of the default mode network. This impairment might be principally due to the disruption of the mechanisms underlying self-inhibition and neuronal oscillations in the posterior cingulate cortex.

Dataset Information

Richness in Functional Connectivity Depends on the Neuronal Integrity within the Posterior Cingulate Cortex.

Publications

Richness in Functional Connectivity Depends on the Neuronal Integrity within the Posterior Cingulate Cortex.

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