The Trend of Disruption in the Functional Brain Network Topology of Alzheimer’s Disease

Alzheimer’s disease (AD) is a progressive disorder associated with cognitive dysfunction that alters the brain’s functional connectivity. Assessing these alterations has become a topic of increasing interest. However, a few studies have examined different stages of AD from a complex network perspective that cover different topological scales. This study used resting state fMRI data to analyze the trend of functional connectivity alterations from a cognitively normal (CN) state through early and late mild cognitive impairment (EMCI and LMCI) and to Alzheimer’s disease. The analyses had been done at the local (hubs and activated links and areas), meso (clustering, assortativity, and rich-club), and global (small-world, small-worldness, and efficiency) topological scales. The results showed that the trends of changes in the topological architecture of the functional brain network were not entirely proportional to the AD progression. There were network characteristics that have changed non-linearly regarding the disease progression, especially at the earliest stage of the disease, i.e., EMCI. Further, it has been indicated that the diseased groups engaged somatomotor, frontoparietal, and default mode modules compared to the CN group. The diseased groups also shifted the functional network towards more random architecture. In the end, the methods introduced in this paper enable us to gain an extensive understanding of the pathological changes of the AD process

The trend of disruption in the functional brain network topology of Alzheimer’s disease

Alzheimer’s disease (AD) is a progressive disorder associated with cognitive dysfunction that alters the brain’s functional connectivity. Assessing these alterations has become a topic of increasing interest. However, a few studies have examined different stages of AD from a complex network perspective that cover different topological scales. This study used resting state fMRI data to analyze the trend of functional connectivity alterations from a cognitively normal (CN) state through early and late mild cognitive impairment (EMCI and LMCI) and to Alzheimer’s disease. The analyses had been done at the local (hubs and activated links and areas), meso (clustering, assortativity, and rich-club), and global (small-world, small-worldness, and efficiency) topological scales. The results showed that the trends of changes in the topological architecture of the functional brain network were not entirely proportional to the AD progression. There were network characteristics that have changed non-linearly regarding the disease progression, especially at the earliest stage of the disease, i.e., EMCI. Further, it has been indicated that the diseased groups engaged somatomotor, frontoparietal, and default mode modules compared to the CN group. The diseased groups also shifted the functional network towards more random architecture. In the end, the methods introduced in this paper enable us to gain an extensive understanding of the pathological changes of the AD process

Brain structural and functional alterations related to anxiety in allergic asthma

Psychiatric disorders are common in patients with allergic asthma, and they can have a significant impact on their quality of life and disease control. Recent studies have suggested that there may be potential immune-brain communication mechanisms in asthma, which can activate inflammatory responses in different brain areas, leading to structural and functional alterations and behavioral changes. However, the precise mechanisms underlying these alterations remain unclear. In this paper, we comprehensively review the relevant research on asthma-induced brain structural and functional alterations that lead to the initiation and promotion of anxiety. We summarize the possible pathways for peripheral inflammation to affect the brain's structure and function. Our review highlights the importance of addressing neuropsychiatric disorders in the clinical guidelines of asthma, to improve the quality of life of these patients. We suggest that a better understanding of the mechanisms underlying psychiatric comorbidities in asthma could lead to the development of more effective treatments for these patients

Effect of Rho-kinase inhibition on complexity of breathing pattern in a guinea pig model of asthma.

Asthma represents an episodic and fluctuating behavior characterized with decreased complexity of respiratory dynamics. Several evidence indicate that asthma severity or control is associated with alteration in variability of lung function. The pathophysiological basis of alteration in complexity of breathing pattern in asthma has remained poorly understood. Regarding the point that Rho-kinase is involved in pathophysiology of asthma, in present study we investigated the effect of Rho-kinase inhibition on complexity of respiratory dynamics in a guinea pig model of asthma. Male Dunkin Hartley guinea pigs were exposed to 12 series of inhalations with ovalbumin or saline. Animals were treated by the Rho-kinase inhibitor Y-27632 (1mM aerosols) prior to each allergen challenge. We recorded respiration of conscious animals using whole-body plethysmography. Exposure to ovalbumin induced lung inflammation, airway hyperresponsiveness and remodeling including goblet cell hyperplasia, increase in the thickness of airways smooth muscles and subepithelial collagen deposition. Complexity analysis of respiratory dynamics revealed a dramatic decrease in irregularity of respiratory rhythm representing less complexity in asthmatic guinea pigs. Inhibition of Rho-kinase reduced the airway remodeling and hyperreponsiveness, but had no significant effect on lung inflammation and complexity of respiratory dynamics in asthmatic animals. It seems that airway hyperresponsiveness and remodeling do not significantly affect the complexity of respiratory dynamics. Our results suggest that inflammation might be the probable cause of shift in the respiratory dynamics away from the normal fluctuation in asthma

Diagram of the custom-built whole-body plethysmograph.

<p>The apparatus included a cylindrical chamber made of transparent Plexiglas. Room air was continuously pumped (4 L/min) into the chamber. A plastic Y-connector was connected to chamber's outlet. One of the exit ports was linked to one input of a differential pressure transducer, and the other input being exposed to the room air. Another port Y-connector was connected to a one input of CO2 sensor. The other input of the CO2 sensor was opened to the room air. The respiratory signals were acquired at the sampling rate of 1 kHz.</p

The trend of disruption in the functional brain network topology of Alzheimer's disease.

Alzheimer's disease (AD) is a progressive disorder associated with cognitive dysfunction that alters the brain's functional connectivity. Assessing these alterations has become a topic of increasing interest. However, a few studies have examined different stages of AD from a complex network perspective that cover different topological scales. This study used resting state fMRI data to analyze the trend of functional connectivity alterations from a cognitively normal (CN) state through early and late mild cognitive impairment (EMCI and LMCI) and to Alzheimer's disease. The analyses had been done at the local (hubs and activated links and areas), meso (clustering, assortativity, and rich-club), and global (small-world, small-worldness, and efficiency) topological scales. The results showed that the trends of changes in the topological architecture of the functional brain network were not entirely proportional to the AD progression. There were network characteristics that have changed non-linearly regarding the disease progression, especially at the earliest stage of the disease, i.e., EMCI. Further, it has been indicated that the diseased groups engaged somatomotor, frontoparietal, and default mode modules compared to the CN group. The diseased groups also shifted the functional network towards more random architecture. In the end, the methods introduced in this paper enable us to gain an extensive understanding of the pathological changes of the AD process

Effect of Rho-kinase inhibition on bronchoalveolar lavage (BAL) inflammatory cells.

<p>Total inflammatory cell (a) and eosinophils (b). *** p<0.001 compared to saline. Data were analyzed by a one-way ANOVA, with the Bonferroni post-test.</p

Effect of Rho-kinase inhibition on airway remodeling and inflammation.

<p>(a), immunohistofluorescence staining to illustrate expression of α-SMA (Scale bar 100 μm); (b), Masson trichrome staining to identify subepithelial collagen deposition (Scale bar 50 μm); (c), hematoxylin and eosin (H&E) staining to detect peribronchial inflammatory cell infiltration (Scale bar 50 μm). (d), periodic acid-Schiff (PAS) staining to assess epithelial goblet cells (Scale bar 20 μm).</p

mRNA expression of TNF-α (a) and IL-13 (b) in the lung of experimental groups.

<p>* p<0.05 and ** p<0.01 compared to Saline group. Data were analyzed by a Kruskal–Wallis test with a Dunn’s post-test.</p

Effect of Rho-kinase inhibition on synchronization between IBI and RV.

<p>* p<0.01 compared to saline group. Data was analyzed by one-way ANOVA with the Bonferroni post-test. IBI, inter-breath interval; RV, respiratory volume; Cross-SampEn, cross-sample entropy.</p