Reduced cerebral cortex thickness is related to overexpression of exosomal miR-146a-5p in medication-free patients with major depressive disorder.

BACKGROUND: Previous studies have confirmed that miR-146a-5p overexpression suppresses neurogenesis, thereby enhancing depression-like behaviors. However, it remains unclear how miR-146a-5p dysregulation produces in vivo brain structural abnormalities in patients with major depressive disorder (MDD). METHODS: In this case-control study, we combined cortical morphology analysis of magnetic resonance imaging (MRI) and miR-146a-5p quantification to investigate the neuropathological effect of miR-146a-5p on cortical thickness in MDD patients. Serum-derived exosomes that were considered to readily cross the blood-brain barrier and contain miR-146a-5p were isolated for miRNA quantification. Moreover, follow-up MRI scans were performed in the MDD patients after 6 weeks of antidepressant treatment to further validate the clinical relevance of the relationship between miR-146a-5p and brain structural abnormalities. RESULTS: In total, 113 medication-free MDD patients and 107 matched healthy controls were included. Vertex-vise general linear model revealed miR-146a-5p-dependent cortical thinning in MDD patients compared with healthy individuals, i.e., overexpression of miR-146a-5p was associated with reduced cortical thickness in the left orbitofrontal cortex (OFC), anterior cingulate cortex, bilateral lateral occipital cortices (LOCs), etc. Moreover, this relationship between baseline miR-146a-5p and cortical thinning was nonsignificant for all regions in the patients who had received antidepressant treatment, and higher baseline miR-146a-5p expression was found to be related to greater longitudinal cortical thickening in the left OFC and right LOC. CONCLUSIONS: The findings of this study reveal a relationship between miR-146a-5p overexpression and cortical atrophy and thus may help specify the in vivo mediating effect of miR-146a-5p dysregulation on brain structural abnormalities in patients with MDD.

In Vivo Structural and Functional Abnormalities of the Striatums Is Related to Decreased Astrocytic BDNF in Itpr2-/- Mice Exhibiting Depressive-Like Behavior.

Background: Previous researches indicate that Itpr2 -/- mice (inositol 1,4,5-trisphosphate receptor type 2 knockout mice) show depressive-like symptoms; however, little is known regarding the in vivo neurobiological effect of Itpr2 as well as the specific pattern of brain abnormalities in Itpr2 -/- mice. Methods/Materials. First, behavioral tests, structural magnetic resonance imaging (MRI), and resting-state functional MRI were performed on Itpr2 -/- mice and matched healthy controls. Voxel-based morphometry and seed-based voxel-wise functional connectivity (FC) were, respectively, calculated to assess the gray matter volume and the functional activities of the brain in vivo. Second, the sample of relevant changed brain regions was extracted to detect the expression of BDNF. Finally, to further validate the relationship between Itpr2 deficiency and the observed brain abnormalities, we performed Western blotting to detect the expression of pro-BDNF and mBDNF in Itpr2 -/- C8-D1A (a type of astrocyte). Results: Compared with controls, Itpr2 -/- mice showed depressive-like behaviors as well as significantly lower gray matter volume in striatums mainly, periaqueductal GM, and the right frontoparietal cortices as well as lower striatal-hippocampal and striatal-right parietal cortex (mainly for the primary and secondary somatosensory cortex) FC. Moreover, decreased expression of mBDNF was found in both sample tissues of the striatum in Itpr2 -/- mice and Itpr2 -/- C8-D1A. Conclusion: By combining biochemistry and MR analyses, this study provides evidences to support that the Itpr2-related neuropathological effect is possibly mediated by the striatal abnormality associated with dysfunctional astrocytes in Itpr2 -/- mice in vivo, thus may help us better understand underlying mechanisms of Itpr2 deficiency as well as its relation to depressive-like behavior.

Effect of selective serotonin reuptake inhibitor on prefrontal-striatal connectivity is dependent on the level of TNF-α in patients with major depressive disorder.

BACKGROUND: We hypothesize that the tumor necrosis factor-α (TNF-α) may play a role in disturbing the effect of selective serotonin reuptake inhibitor (SSRI) on the striatal connectivity in patients with major depressive disorder (MDD). METHODS: We performed a longitudinal observation by combining resting-state functional magnetic resonance imaging (rs-fMRI) and biochemical analyses to identify the abnormal striatal connectivity in MDD patients, and to evaluate the effect of TNF-α level on these abnormal connectivities during SSRI treatment. Eighty-five rs-fMRI scans were collected from 25 MDD patients and 35 healthy controls, and the scans were repeated for all the patients before and after a 6-week SSRI treatment. Whole-brain voxel-wise functional connectivity (FC) was calculated by correlating the rs-fMRI time courses between each voxel and the striatal seeds (i.e. spherical regions placed at the striatums). The level of TNF-α in serum was evaluated by Milliplex assay. Factorial analysis was performed to assess the interaction effects of 'TNF-α × treatment' in the regions with between-group FC difference. RESULTS: Compared with controls, MDD patients showed significantly higher striatal FC in the medial prefrontal cortex (MPFC) and bilateral middle/superior temporal cortices before SSRI treatment (p < 0.001, uncorrected). Moreover, a significant interaction effect of 'TNF-α × treatment' was found in MPFC-striatum FC in MDD patients (p = 0.002), and the significance remained after adjusted for age, gender, head motion, and episode of disease. CONCLUSION: These findings provide evidence that treatment-related brain connectivity change is dependent on the TNF-α level in MDD patients, and the MPFC-striatum connectivities possibly serve as an important target in the brain.

NIR-activated Janus nanomotors with promoted tumor permeability for synergistic photo-immunotherapy.

Nanoparticle-based photo-immunotherapy has become an attractive strategy to eliminate tumors and activate host immune responses. However, the therapeutic efficacy is heavily restricted by low tumoral penetration and immunosuppressive tumor microenvironment (TME). Herein, near infrared laser (NIR)-propelled Janus nanomotors were presented for deep tumoral penetration, photothermal tumor ablation and photothermal-triggered augmented immunotherapy. The Janus nanomotors (AuNR/PMO@CPG JNMs) were constructed with gold nanorods (AuNR) and periodic mesoporous organo-silica nanospheres (PMO), followed by loading of immune adjuvant (CPG ODNs). Under NIR irradiation, the nanomotors exhibited superior photothermal effect, which produced active motion with a speed of 19.3 µm/s for deep tumor penetration and accumulation in vivo. Moreover, the good photothermal heating also benefited effective photothermal ablation to trigger immunogenic cell death (ICD). Subsequently, the ICD effect promoted the release of tumor-associated antigens (TAAs) and damage associated molecular patterns (DAMPs), and further generated abundant tumor vaccines in situ for reprograming the immunosuppressive TME in combination with CPG ODNs to inhibit tumor growth. As a result, a notable in vivo synergistic therapeutic effect was realized on CT26-bearing mice by combining photothermal therapy-induced ICD with modulation of immunosuppressive TME. Thus, we believe that the synthesized nanomotors can provide a new inspect to boost photothermal therapy-induced ICD in tumor immunotherapy. STATEMENT OF SIGNIFICANCE: Nanoparticle-based synergistic photo-immunotherapy has become a popular strategy to eliminate tumors and activate host immune responses. However, the therapeutic efficacy is heavily restricted by low tumoral penetration and immunosuppressive tumor microenvironment (TME). In this work, near infrared laser (NIR)-propelled Janus nanomotors were presented for deep tumoral penetration, photothermal tumor ablation and photothermal-triggered augmented immunotherapy. Under NIR irradiation, the nanomotors exhibited a superior photothermal effect, which produced active motion for deep tumor penetration and accumulation in vivo. Moreover, good photothermal heating also facilitated effective photothermal ablation to trigger immunogenic cell death (ICD), which promoted the release of tumor-associated antigens and damage-associated molecular patterns (DAMPs), and further generated abundant tumor vaccines in situ for reprograming the immunosuppressive TME to inhibit tumor growth.

Exosomal miR-1202 mediates Brodmann Area 44 functional connectivity changes in medication-free patients with major depressive disorder: An fMRI study.

Previous large-sample postmortem study revealed that the expression of miR-1202 in brain tissues from Brodmann area 44 (BA44) was dysregulated in patients with major depressive disorder (MDDs). However, the specific in vivo neuropathological mechanism of miR-1202 as well as its interplay with BA44 circuits in the depressed brain are still unclear. Here, we performed a case-control study with imaging-genetic approach based on resting-state functional magnetic resonance imaging (MRI) data and miR-1202 quantification from 110 medication-free MDDs and 102 healthy controls. Serum-derived circulating exosomes that readily cross the blood-brain barrier were isolated to quantify miR-1202. For validation, repeated MR scans were performed after a six-week follow-up of antidepressant treatment on a cohort of MDDs. Voxelwise factorial analysis revealed two brain areas (including the striatal-thalamic region) in which the effect of depression on the functional connectivity with BA44 was significantly dependent on the expression level of exosomal miR-1202. Moreover, longitudinal change of the BA44 connectivity with the striatal-thalamic region in MDDs after antidepressant treatment was found to be significantly related to the level of miR-1202 expression. These findings revealed that the in vivo neuropathological effect of miR-1202 dysregulation in depression is possibly exerted by mediating neural functional abnormalities in BA44-striatal-thalamic circuits.

Deciphering the neural mechanisms of miR-134 in major depressive disorder with population-based and person-specific imaging transcriptomic techniques.

MiR-134 has emerged as a potential molecular biomarker for the detection and management of major depressive disorder (MDD). Nevertheless, the specific effects of miR-134 as a regulatory element on brain function and its implications for the clinical presentation of MDD are not yet fully understood. In order to investigate the potential neural mechanisms that contribute to the relationship between miR-134 and MDD, we employed a parallel two-stage cross-scale multi-omics approach. This involved utilizing the anterior cingulate cortex (ACC) functional connectivity as a means to connect microscopic molecular structures with macroscopic brain function in two separate cohorts: the MDD-I dataset (56 MDD patients and 51 healthy controls) and the MDD-II dataset (57 MDD patients and 52 healthy controls). We found a stable ACC functional dysconnectivity pattern of MDD and established the hierarchical cross-scale association from molecular organizations of miR-134 target genes to macroscopic brain functional dysconnectivity and associated behavior, as revealed by population-based analysis. Additionally, our person-specific imaging transcriptomic study revealed that individual exosomal miR-134 expression levels impact on individual clinical symptoms of MDD by modulating ACC-related functional dysconnectivity. Together, our findings provide compelling evidence of the correlation between miR-134 and depression across multi scales within the gene-brain-behavior context.

Cortical Short-Range Fiber Connectivity and Its Association With Deep Brain White Matter Hyperintensities in Older Diabetic People With Low Serum Vitamin B12.

Although previous studies have indicated that older people with diabetes mellitus (DM) had an approximately two times larger white matter hyperintensity (WMH) load than those without DM, the influence of WMHs on cognition is uncertain and inconsistent in the literature. It is unclear whether the short-range fibers in the juxtacortical region, traditionally considered to be spared from WMH pathology, are enhanced as an adaptive response to deep WM degeneration in older diabetic people with normal cognition. Moreover, the specific effect of vitamin B12 deficiency, commonly accompanied by DM, remains to be investigated. This study implemented a specialized analysis of the superficial cortical short-range fiber connectivity density (SFiCD) based on a data-driven framework in 70 older individuals with DM and low serum vitamin B12. Moreover, the effects of time and vitamin B12 supplementation were assessed based on a randomized placebo-controlled trial in 59 individuals. The results demonstrated a higher SFiCD in diabetic individuals with a higher deep WMH load. Additionally, a significant interaction between DWMH load and homocysteine on SFiCD was found. During the 27-month follow-up period, a longitudinal increase in the SFiCD was observed in the bilateral frontal cortices. However, the observed longitudinal SFiCD change was not dependent on vitamin B12 supplementation; thus, the specific reason for the longitudinal cortical short fiber densification may need further study. Overall, these findings may help us better understand the neurobiology of brain plasticity in older patients with DM, as well as the interplay among DM, WMH, and vitamin B12 deficiency.

Simultaneously decreased temporal variability and enhanced variability-strength coupling of emotional network connectivities are related to positive symptoms in patients with schizophrenia.

We hypothesize that decreased temporal variability of emotional network connectivities, corresponding to a continual state of hyperactivity, may play a role in mediating symptoms in schizophrenia. Resting-state magnetic resonance data were collected from 64 subjects, including 21 positive symptom profile schizophrenia patients (PSZ group), 19 negative symptom profile schizophrenia patients (NSZ group), and 24 healthy controls. The emotional brain network was defined based on the coordinates obtained from multi-level kernel density analysis. The temporal variability of intra-network functional connectivities (FCs) was calculated by constructing networks from blood oxygen level-dependent signals at successive, non-overlapping time windows, and was compared between groups. The results showed that the mean FC-variability of the whole emotional network (P = 0.021), and the FC-variabilities in the bilateral anterior insula (both, P < 0.001) were significantly decreased in the PSZ group compared with the control and NSZ groups. Abnormally enhanced negative coupling between variability and FC strength (V-S coupling) was observed in the PSZ group (P = 0.027). In summary, this study found a relation between the positive symptoms of schizophrenia and decreased variability of emotional network connectivities. These findings may help us better understand the neurobiological effect of the time-varying properties of the brain network in schizophrenia patients, and the underlying relation to the generation of psychosis.

Ventral and dorsal visual pathways exhibit abnormalities of static and dynamic connectivities, respectively, in patients with schizophrenia.

Previous studies suggest that schizophrenia-related visual perceptual abnormalities are primarily attributed to deficits of the dorsal rather than ventral visual pathway. In this study, we comparatively explored changes in dorsal and ventral networks in schizophrenia patients in both static and dynamic functional connectivity (FC). Resting-state MR scans were acquired for forty schizophrenia patients and twenty-four healthy controls matched for age and gender. The dorsal and ventral visual networks were defined based on the resultant coordinates from activation likelihood estimation analyses. Static and dynamic network properties were calculated based on the full-range and segmented blood oxygen level dependent time series, respectively. The results indicated that the ventral and dorsal visual networks exhibited abnormalities in static FC and dynamic FC, respectively, in the schizophrenia group. Static FC assessments in the ventral visual network showed a significantly decreased clustering coefficient and shortened characteristic path length in patients with schizophrenia. Dynamic FC assessments in the dorsal visual network showed significantly higher mean temporal variability (p = 0.026) and higher regional FC variability of the right fusiform gyrus (p < 0.001) in patients with schizophrenia, and the latter was correlated with the total and negative scores of the Positive and Negative Syndrome Scale. In summary, this study reveals differential patterns of connectivity abnormalities of the ventral and dorsal visual networks in patients with schizophrenia. These preliminary evidences may help us better interpret the mechanisms underlying visual perceptual impairments in patients with schizophrenia and their relationship with psychosis.

More optimal but less regulated dorsal and ventral visual networks in patients with major depressive disorder.

Previous studies indicate that major depressive disorder (MDD) can profoundly modify the visual cortices as well as the visuo-attentional systems of brain. However, little is known on the specific pattern of the whole-network-level abnormalities. In this study, resting-state functional magnetic resonance imaging data were collected from 159 participants, including 86 medication-free MDD patients and 73 matched healthy controls. The dorsal/ventral visual networks were defined based on our previously published brain coordinates from activation likelihood estimation analyses. The static and dynamic network properties were respectively calculated and compared between MDD and control groups. Moreover, the inter-network connectivities quantified using the multivariate distance correlation between the dorsal attention network (DAN) and the two visual networks were also analyzed. Results indicated that both of the two visual networks in MDD were found with significantly increased clustering coefficient (dorsal: p = 0.002; ventral: p = 0.004) and higher small-worldness (dorsal: p = 0.001; ventral: p = 0.002) as compared with control group. A higher mean variability of dynamic functional connectivity was found in both two networks in MDDs (dorsal: p < 0.001; ventral: p = 0.001). Moreover, the two visual networks in MDD group showed decreased inter-network connectivities to DAN (dorsal: p = 0.004; ventral: p = 0.013). Taken together, these results may support that the ventral and dorsal visual systems under the pathological effect of depression are possibly characterized by a status of increased autonomy, i.e., a more optimal, economical, and efficient intra-network organization combining with increased independency and receiving less outside regulation from attention network, thus indicating the increased functional role of the brain visual systems in MDD.

Modified Xiaoyao San ameliorates depressive-like behaviors by triggering autophagosome formation to alleviate neuronal apoptosis.

Major depressive disorder (MDD) affects ˜16% of the world population. Chronic stressors contribute to reduced hippocampal volumes and increase the risk of developing MDD. Our previous work showed that XYS ameliorates social isolation and chronic unpredictable mild stress (CUMS) induced depressive-like behaviors in rats by regulating hypothalamic-pituitary-adrenal hyperactivation, locus coeruleus -norepinephrine activity and kynurenine/5-hydroxytryptamin balance. Here, we report that CUMS & isolation-treated mice exhibit depressive-like behaviors and show a phenotype of mixed apoptosis/autophagy characteristic in mice hippocampus in vivo. Modified Xiaoyao San (MXS) significantly ameliorates CUMS & social isolation-induced anhedonia, loss of interests, psychomotor retardation and behavioral despair. It suppresses the apoptosis by downregulaing condensation of heterochromatin and reducing hippocampal TdT-mediated dUTP Nick-End Labeling (TUNEL)-positive cells. MSX significantly inhibits mitochondrial outer membrane permeabilization (MOMP) reduces the release of cytochrome C and the shift of apoptosis inducing factor (AIF) from mitochondria to nucleus. Further, it stimulates the formation of autophagosomes and activates the expression of Atg5 and LC3II. Combined silencing of Atg5 and Atg7 dampens MOMP and impaired the anti-apoptotic effects of MXS. In conclusion, MXS ameliorates depressive-like behaviors by triggering autophagy to alleviate neuronal apoptosis. MXS is an effective supplement for MDD treatment, and can be harnessed to enhance autophagy and synergize with antidepressant action.

Adult pancreatoblastoma: A case report and clinicopathological review of the literature.

PURPOSE: Our purpose was to report a case of adult pancreatoblastoma, and review the literature in order to assist clinicians in the management of the disease. MATERIALS AND METHODS: The demographic, clinical, and imaging findings of 41 patients with pathologically proven pancreatoblastoma from 1986 to 2017 identified in PubMed were reviewed. The key words used for searching PubMed were: "pancreatoblastoma", "pancreatic tumor", and "adult pancreatoblastoma." We also reported the details of a case of adult pancreatoblastoma treated at our institution. RESULTS: We identified 41 cases of adult pancreatoblastomas, and the mean age at diagnosis was 41.4 ±â€¯17.4 years. Pancreatoblastomas occurred in the pancreatic head in 48.4% of patients, and in 39.0% of cases the tumor was >8 cm in diameter at diagnosis. Patient age and tumor size were similar between males and females (P = 0.59; P = 0.32, respectively). Metastases was present in 17 of the 41 adult patients (41.5%). No significant difference in age, sex, tumor size, and tumor location was found between patients with and without metastases (P = 0.57, 0.58, 0.64, 0.39, respectively). CONCLUSION: Preoperative diagnosis of adult pancreatoblastoma is difficult because of the heterogeneous, variable cellular differentiation and atypical clinical and imaging features. A pancreatoblastoma should be considered when tumors in the pancreas are solid and cystic.

Altered topological organization of high-level visual networks in Alzheimer's disease and mild cognitive impairment patients.

Altered regional activation of high-level visual (HLV) cortices in patients with Alzheimer's disease (AD) or mild cognitive impairment (MCI) has been well documented in previous fMRI studies, which led us to investigate the underlying alteration of the HLV networks in the terms of intrinsic interaction and topological organization. First, the activation likelihood estimation, a coordinate-based meta-analysis approach, was used to define the cortical regions/nodes included in HLV networks of "what" and "where" visions. Secondly, the acquired HLV regions were used as seeds to calculate their interregional resting-state functional connectivities (RSFCs) based on the temporal correlation of rs-functional MRI (rs-fMRI) time series. Here, the rs-fMRI data of AD (n=30), late MCI (n=35), early MCI (n=52) and matched healthy controls (n=44) were obtained from the Alzheimer's Disease Neuroimaging Initiative dataset. Finally, based on the calculated pair-wise RSFCs, the "what" and "where" HLV networks were respectively constructed, and their topological properties were calculated and analyzed among groups using the graph theory method. The results demonstrated increased clustering coefficient combined with a prolonged characteristic path length of the "where" visual network in AD patients. No significant alternation of the "what" visual network was found among the groups. These results suggest that the abnormality of the HLV networks could be a late-stage outcome in AD and that the "where" visual network may be more susceptible to the AD-related neuropathological changes than the "what" visual network. In addition, the dysfunction of the "where" network is found to be characterized by a decreased integration combined with an increased local segregation.

The brain effects of laser acupuncture at thirteen ghost acupoints in healthy individuals: A resting-state functional MRI investigation.

Acupuncture at thirteen ghost acupoints (TGA) was an effective treatment of neuropsychological disorders. However, the underlying neurological mechanisms of acupuncture at the TGA have not been revealed by modern scientific technologies. As laser acupuncture emerges with the painless and noninvasive advantages and the functional magnetic resonance imaging (fMRI) allows us to investigate the activation of the brain in vivo, we performed the preliminary study to investigate the relation to brain effects of acupuncture at TGA based on resting-state fMRI (rs-fMRI). Twenty one healthy subjects underwent rs-fMRI scan before and after acupuncturing TGA (except HI11 and CV1). The regional homogeneity (ReHo) values and the amplitude of low-frequency fluctuation (ALFF) values were evaluated within the whole brain and compared before and after laser stimulation of TGA. We found increased ReHo/ALFF value in serious brain regions, including right inferior occipital gyrus, bilateral middle occipital gyrus, left inferior temporal gyrus, and bilateral postcentral gyrus, after acupuncture. While, significantly decreased ReHo/ALFF value was found in the cerebellum, left superior medial frontal gyrus, left precuneus, right middle temporal gyrus, right middle frontal gyrus and left superior parietal lobule after laser stimulation. The changes in brain spontaneous function after laser acupuncture may suggest that acupuncturing at TGA may have the potential modulating effect of the cognitive functions. These preliminary findings of the changes of brain patterns at resting-state after TGA stimulation may lay the groundwork for further studies on its therapeutic effect in some neuropsychological disease models.

Mapping the "What" and "Where" Visual Cortices and Their Atrophy in Alzheimer's Disease: Combined Activation Likelihood Estimation with Voxel-Based Morphometry.

The human cortical regions for processing high-level visual (HLV) functions of different categories remain ambiguous, especially in terms of their conjunctions and specifications. Moreover, the neurobiology of declined HLV functions in patients with Alzheimer's disease (AD) has not been fully investigated. This study provides a functionally sorted overview of HLV cortices for processing "what" and "where" visual perceptions and it investigates their atrophy in AD and MCI patients. Based upon activation likelihood estimation (ALE), brain regions responsible for processing five categories of visual perceptions included in "what" and "where" visions (i.e., object, face, word, motion, and spatial visions) were analyzed, and subsequent contrast analyses were performed to show regions with conjunctive and specific activations for processing these visual functions. Next, based on the resulting ALE maps, the atrophy of HLV cortices in AD and MCI patients was evaluated using voxel-based morphometry. Our ALE results showed brain regions for processing visual perception across the five categories, as well as areas of conjunction and specification. Our comparisons of gray matter (GM) volume demonstrated atrophy of three "where" visual cortices in late MCI group and extensive atrophy of HLV cortices (25 regions in both "what" and "where" visual cortices) in AD group. In addition, the GM volume of atrophied visual cortices in AD and MCI subjects was found to be correlated to the deterioration of overall cognitive status and to the cognitive performances related to memory, execution, and object recognition functions. In summary, these findings may add to our understanding of HLV network organization and of the evolution of visual perceptual dysfunction in AD as the disease progresses.

Identifying the Alteration Patterns of Brain Functional Connectivity in Progressive Mild Cognitive Impairment Patients: A Longitudinal Whole-Brain Voxel-Wise Degree Analysis.

Patients with mild cognitive impairment (MCI) are at high risk for developing Alzheimer's disease (AD), while some of them may remain stable over decades. The underlying mechanism is still not fully understood. In this study, we aimed to explore the connectivity differences between progressive MCI (PMCI) and stable MCI (SMCI) individuals on a whole-brain scale and on a voxel-wise basis, and we also aimed to reveal the differential dynamic alteration patterns between these two disease subtypes. The resting-state functional magnetic resonance images of PMCI and SMCI patients at baseline and year-one were obtained from the Alzheimer's Disease Neuroimaging Initiative dataset, and the progression was determined based on a 3-year follow-up. A whole-brain voxel-wise degree map that was calculated based on graph-theory was constructed for each subject, and then the cross-sectional and longitudinal analyses on the degree maps were performed between PMCI and SMCI patients. In longitudinal analyses, compared with SMCI group, PMCI group showed decreased long-range degree in the left middle occipital/supramarginal gyrus, while the short-range degree was increased in the left supplementary motor area and middle frontal gyrus and decreased in the right middle temporal pole. A significant longitudinal alteration of decreased short-range degree in the right middle occipital was found in PMCI group. Taken together with previous evidence, our current findings may suggest that PMCI, compared with SMCI, might be a "severe" presentation of disease along the AD continuum, and the rapidly reduced degree in the right middle occipital gyrus may have indicative value for the disease progression. Moreover, the cross-sectional comparison results and corresponding receiver-operator characteristic-curves analyses may indicate that the baseline degree difference is not a good predictor of disease progression in MCI patients. Overall, these findings may provide objective evidence and an indicator to characterize the progression-related brain connectivity changes in MCI patients.

Anomalous gray matter structural networks in patients with hepatitis B virus-related cirrhosis without overt hepatic encephalopathy.

BACKGROUND AND PURPOSE: Increasing evidence suggests that cirrhosis may affect the connectivity among different brain regions in patients before overt hepatic encephalopathy (OHE) occurs. However, there has been no study investigating the structural reorganization of these altered connections at the network level. The primary focus of this study was to investigate the abnormal topological organization of the structural network in patients with hepatitis B virus-related cirrhosis (HBV-RC) without OHE using structural MRI. METHODS: Using graph theoretical analysis, we compared the global and regional topological properties of gray matter structural networks between 28 patients with HBV-RC without OHE and 30 age-, sex- and education-matched healthy controls. The structural correlation networks were constructed for the two groups based on measures of gray matter volume. RESULTS: The brain network of the HBV-RC group exhibited a significant decrease in the clustering coefficient and reduced small-worldness at the global level across a range of network densities. Regionally, brain areas with altered nodal degree/betweenness centrality were observed predominantly in association cortices (frontal and temporal regions) (p < 0.05, uncorrected), including a significantly decreased nodal degree in the inferior temporal gyrus (p < 0.001, uncorrected). Furthermore, the HBV-RC group exhibited a loss of association hubs and the emergence of an increased number of non-association hubs compared with the healthy controls. CONCLUSION: The results of this large-scale gray matter structural network study suggest reduced topological organization efficiency in patients with HBV-RC without OHE. Our findings provide new insight concerning the mechanisms of neurobiological reorganization in the HBV-RC brain from a network perspective.

MR imaging of cerebral extraventricular neurocytoma: a report of 9 cases.

Extraventricular neurocytoma is a rare entity, most frequently occurring in brain parenchyma outside the ventricular system. The purpose of this study was to characterize the MR imaging findings in a series of 9 patients with EVN verified by results of pathologic examination. All 9 EVNs were solitary and intracranially located. Eight lesions were well demarcated, and 3 showed intratumoral hemorrhage. The solid parts of 7 tumors were primarily isointense on T1-weighted images and heterogeneously enhanced on T1WI with contrast. Although cerebral EVNs can present a wide spectrum of appearances on MR, the imaging patterns appear to vary according to anatomic location and cellularity. Lesions in frontal or parietal lobes often present as well-demarcated large masses with cystic degeneration, hemorrhage, mild-to-moderate edema, and inhomogeneous enhancement. Moreover, the general isointensity of the solid parts of EVN on T1WI may be of some specificity.