Brain Network Characterization of Preterm Infants With Bronchopulmonary Dysplasia.

BACKGROUND: Bronchopulmonary dysplasia (BPD) affects the microstructure of white matter in preterm infants, but its influence on the changes of the brain structural network has not been elaborated. This study aims to investigate the connectivity characteristics of the brain structural network of BPD by using diffusion tensor imaging. METHODS: Thirty-three infants with BPD and 26 infants without BPD were enrolled in this study. Brain structural networks were constructed utilizing automated anatomic labeling mapping by tracing the fibers between each pair of regions in individual space. We calculated network metrics such as global efficiency, local efficiency, clustering coefficients, characteristic path length, and small-worldness. Then we compared the network metrics of these infants with those of 57 healthy term infants of comparable postmenstrual age at magnetic resonance imaging scan. Finally, network-based statistics was used to analyze the differences in brain network connectivity between the groups with and without BPD. RESULTS: Preterm infants with BPD had higher local efficiency and clustering coefficient, lower global efficiency, and longer characteristic path length. Also, preterm infants with BPD had decreased strength of limbic connections mainly in four brain regions: the left lingual gyrus, the left calcarine fissure and surrounding cortex, the right parahippocampal gyrus, and the left precuneus. CONCLUSIONS: Our findings suggest that preterm infants with BPD have lower network integration and higher segregation at term-equivalent age, which may reflect a compensatory mechanism. In addition, BPD affects brain regions involved in visual as well as cognitive functions; these findings provide a new approach to diagnose potential brain damage in preterm infants with BPD.

Electroacupuncture Enhances the Functional Connectivity of Limbic System to Neocortex in the 5xFAD Mouse Model of Alzheimer's Disease.

Our previous study revealed that acupuncture may exhibit therapeutic effects on Alzheimer's disease (AD) through the activation of metabolism in memory-related brain regions. However, the underlying functional mechanism remains poorly understood and warrants further investigation. In this study, we used resting-state functional magnetic resonance imaging (rsfMRI) to explore the potential effect of electroacupuncture (EA) on the 5xFAD mouse model of AD. We found that the EA group exhibited significant improvements in the number of platforms crossed and the time spent in the target quadrant when compared with the Model group (p < 0.05). The functional connectivity (FC) of left hippocampus (Hip) was enhanced significantly among 12 regions of interest (ROIs) in the EA group (p < 0.05). Based on the left Hip as the seed point, the rsfMRI analysis of the entire brain revealed increased FC between the limbic system and the neocortex in the 5xFAD mice after EA treatment. Additionally, the expression of amyloid-ß(Aß) protein and deposition in the Hip showed a downward trend in the EA group compared to the Model group (p < 0.05). In conclusion, our findings indicate that EA treatment can improve the learning and memory abilities and inhibit the expression of Aß protein and deposition of 5xFAD mice. This improvement may be attributed to the enhancement of the resting-state functional activity and connectivity within the limbic-neocortical neural circuit, which are crucial for cognition, motor function, as well as spatial learning and memory abilities in AD mice.

Lateralized brunt of sleep deprivation on white matter injury in a rat model of Alzheimer's disease.

Sleep disturbance is a recognized risk factor for Alzheimer's disease (AD), but the underlying micro-pathological evidence remains limited. To bridge this gap, we established an amyloid-ß oligomers (AßO)-induced rat model of AD and subjected it to intermittent sleep deprivation (SD). Diffusion tensor imaging (DTI) and transmission electron microscopy were employed to assess white matter (WM) integrity and ultrastructural changes in myelin sheaths. Our findings demonstrated that SD exacerbated AßO-induced cognitive decline. Furthermore, we found SD aggravated AßO-induced asymmetrical impairments in WM, presenting with reductions in tract integrity observed in commissural fibers and association fasciculi, particularly the right anterior commissure, right corpus callosum, and left cingulum. Ultrastructural changes in myelin sheaths within the hippocampus and corpus callosum further confirmed a lateralized effect. Moreover, SD worsened AßO-induced lateralized disruption of the brain structural network, with impairments in critical nodes of the left hemisphere strongly correlated with cognitive dysfunction. This work represents the first identification of a lateralized impact of SD on the mesoscopic network and cognitive deficits in an AD rat model. These findings could deepen our understanding of the complex interplay between sleep disturbance and AD pathology, providing valuable insights into the early progression of the disease, as well as the development of neuroimaging biomarkers for screening early AD patients with self-reported sleep disturbances. Enhanced understanding of these mechanisms may pave the way for targeted interventions to alleviate cognitive decline and improve the quality of life for individuals at risk of or affected by AD.

Harmonizing T1-Weighted Images to Improve Consistency of Brain Morphology Among Different Scanner Manufacturers in Alzheimer's disease.

BACKGROUND: Brain MRI scanner variability can introduce bias in measurements. Harmonizing scanner variability is crucial. PURPOSE: To develop a harmonization method aimed at removing scanner variability, and to evaluate the consistency of results in multicenter studies. STUDY TYPE: Retrospective. POPULATION: Multicenter data from 170 healthy participants (males/females = 98/72; age = 73.8 ± 7.3) and 170 Alzheimer's disease patients (males/females = 98/72; age = 76.2 ± 8.5) were compared with reference data from another 340 participants. FIELD STRENGTH/SEQUENCE: 3-T, magnetization prepared rapid gradient echo and turbo field echo; 1.5-T, inversion recovery prepared fast spoiled gradient echo T1-weighted sequences. ASSESSMENT: Gray matter (GM) brain images, obtained through segmentation of T1-weighted images, were utilized to evaluate the performance of the harmonization method using common orthogonal basis extraction (HCOBE) and four other methods (removal of artificial voxel effect by linear regression, RAVEL; Z_score; general linear model, GLM; ComBat). Linear discriminant analysis (LDA) was used to access the effectiveness of different methods in reducing scanner variability. The performance of harmonization methods in preserving GM volumes heterogeneity was evaluated by the similarity of the relationship between GM proportion and age in the reference and multicenter data. Furthermore, the consistency of the harmonized multicenter data with the reference data were evaluated based on classification results (train/test = 7/3) and brain atrophy. STATISTICAL TESTS: Two-sample t-tests, area under the curve (AUC), and Dice coefficients were used to analyze the consistency of results from the reference and harmonized multicenter data. A P-value <0.01 was considered statistically significant. RESULTS: HCOBE reduced the scanner variability from 0.09 before harmonization to 0.003 (ideal: 0, RAVEL/Z_score/GLM/ComBat = 0.087/0.003/0.006/0.013). GM volumes showed no significant difference (P = 0.52) between the reference and HCOBE-harmonized multicenter data. Consistency evaluation showed that AUC values of 0.95 for both reference and HCOBE-harmonized multicenter data (RAVEL/Z_score/GLM/ComBat = 0.86/0.86/0.84/0.89), and the Dice coefficient increased from 0.73 before harmonization to 0.82 (ideal: 1, RAVEL/Z_score/GLM/ComBat = 0.39/0.64/0.59/0.74). DATA CONCLUSION: HCOBE may help to remove scanner variability and could improve the consistency of results in multicenter studies. LEVEL OF EVIDENCE: 2 TECHNICAL EFFICACY STAGE: 1.

Combination of fMRI and PET reveals the beneficial effect of three-phase enriched environment on post-stroke memory deficits by enhancing plasticity of brain connectivity between hippocampus and peri-hippocampal cortex.

AIM: The three-phase enriched environment (EE) intervention paradigm has been shown to improve learning and memory function after cerebral ischemia, but the neuronal mechanisms are still unclear. This study aimed to investigate the hippocampal-cortical connectivity and the metabolic interactions between neurons and astrocytes to elucidate the underlying mechanisms of EE-induced memory improvement after stroke. METHODS: Rats were subjected to permanent middle cerebral artery occlusion (pMCAO) or sham surgery and housed in standard environment or EE for 30 days. Memory function was examined by Morris water maze (MWM) test. Magnetic resonance imaging (MRI) was conducted to detect the structural and functional changes. [18 F]-fluorodeoxyglucose (FDG) positron emission tomography (PET) was conducted to detect brain energy metabolism. PET-based brain connectivity and network analysis was performed to study the changes of hippocampal-cortical connectivity. Astrocyte-neuron metabolic coupling, including gap junction protein connexin 43 (Cx43), glucose transporters (GLUTs), and monocarboxylate transporters (MCTs), was detected by histological studies. RESULTS: Our results showed EE promoted memory function improvement, protected structure integrity, and benefited energy metabolism after stroke. More importantly, EE intervention significantly increased functional connectivity between the hippocampus and peri-hippocampal cortical regions, and specifically regulated the level of Cx43, GLUTs and MCTs in the hippocampus and cortex. CONCLUSIONS: Our results revealed the three-phase enriched environment paradigm enhanced hippocampal-cortical connectivity plasticity and ameliorated post-stroke memory deficits. These findings might provide some new clues for the development of EE and thus facilitate the clinical transformation of EE.

Three-phase Enriched Environment Improves Post-stroke Gait Dysfunction via Facilitating Neuronal Plasticity in the Bilateral Sensorimotor Cortex: A Multimodal MRI/PET Analysis in Rats.

The three-phase Enriched Environment (EE) paradigm has been shown to promote post-stroke functional improvement, but the neuronal mechanisms are still unclear. In this study, we applied a multimodal neuroimaging protocol combining magnetic resonance imaging (MRI) and positron emission tomography (PET) to examine the effects of post-ischemic EE treatment on structural and functional neuroplasticity in the bilateral sensorimotor cortex. Rats were subjected to permanent middle cerebral artery occlusion. The motor function of the rats was examined using the DigiGait test. MRI was applied to investigate the EE-induced structural modifications of the bilateral sensorimotor cortex. [18F]-fluorodeoxyglucose PET was used to detect glucose metabolism. Blood oxygen level-dependent (BOLD)-functional MRI (fMRI) was used to identify the regional brain activity and functional connectivity (FC). In addition, the expression of neuroplasticity-related signaling pathways including neurotrophic factors (BDNF/CREB), axonal guidance proteins (Robo1/Slit2), and axonal growth-inhibitory proteins (NogoA/NgR) as well as downstream proteins (RhoA/ROCK) in the bilateral sensorimotor cortex were measured by Western blots. Our results showed the three-phase EE improved the walking ability. Structural T2 mapping imaging and diffusion tensor imaging demonstrated that EE benefited structure integrity in the bilateral sensorimotor cortex. PET-MRI fused images showed improved glucose metabolism in the corresponding regions after EE intervention. Specifically, the BOLD-based amplitude of low-frequency fluctuations showed that EE increased spontaneous activity in the bilateral motor cortex and ipsilateral sensory cortex. In addition, FC results showed increased sensorimotor connectivity in the ipsilateral hemisphere and increased interhemispheric motor cortical connectivity and motor cortical-thalamic connectivity following EE intervention. In addition, a strong correlation was found between increased functional connectivity and improved motor performance of limbs. Specifically, EE regulated the expression of neuroplasticity-related signaling, involving BDNF/CREB, Slit2/Robo1, as well as the axonal growth-inhibitory pathways Nogo-A/Nogo receptor and RhoA/ROCK in the bilateral sensorimotor cortex. Our results indicated that the three-phase enriched environment paradigm enhances neuronal plasticity of the bilateral sensorimotor cortex and consequently ameliorates post-stroke gait deficits. These findings might provide some new clues for the development of EE and thus facilitate the clinical translation of EE.

Dopaminergic damage pattern predicts phenoconversion time in isolated rapid eye movement sleep behavior disorder.

PURPOSE: The exact phenoconversion time from isolated rapid eye movement (REM) sleep behavior disorder (iRBD) to synucleinopathies remains unpredictable. This study investigated whole-brain dopaminergic damage pattern (DDP) with disease progression and predicted phenoconversion time in individual patients. METHODS: Age-matched 33 iRBD patients and 20 healthy controls with 11C-CFT-PET scans were enrolled. The patients were followed up 2-10 (6.7 ± 2.0) years. The phenoconversion year was defined as the base year, and every 2 years before conversion was defined as a stage. Support vector machine with leave-one-out cross-validation strategy was used to perform prediction. RESULTS: Dopaminergic degeneration of iRBD was found to occur about 6 years before conversion and then abnormal brain regions gradually expanded. Using DDP, area under curve (AUC) was 0.879 (90% sensitivity and 88.3% specificity) for predicting conversion in 0-2 years, 0.807 (72.7% sensitivity and 83.3% specificity) in 2-4 years, 0.940 (100% sensitivity and 84.6% specificity) in 4-6 years, and 0.879 (100% sensitivity and 80.7% specificity) over 6 years. In individual patients, predicted stages correlated with whole-brain dopaminergic levels (r = - 0.740, p < 0.001). CONCLUSION: Our findings suggest that DDP could accurately predict phenoconversion time of individual iRBD patients, which may help to screen patients for early intervention.

Equilibrium Dynamics of Mutually Confined Waves with Signed Analogous Masses.

We report the first experimental realization of equilibrium dynamics of mutually confined waves with signed analogous masses in an optical fiber. Our Letter is mainly demonstrated by considering a mutual confinement between a soliton pair and a dispersive wave experiencing opposite dispersion. The resulting wave-packet complex is found robust upon random perturbation and collision with other waves. The equilibrium dynamics are also extended to scenarios of more than three waves. Our finding may trigger fundamental interest in the dynamics of many-body systems arising from the concept of negative mass, which is promising for new applications based on localized nonlinear waves.

Automatic brain extraction for rat magnetic resonance imaging data using U2-Net.

Objective.Skull stripping is a key step in the pre-processing of rodent brain magnetic resonance images (MRI). This study aimed to develop a new skull stripping method via U2-Net, a neural network model based on deep learning method, for rat brain MRI.Approach.In this study, 599 rats were enrolled and U2-Net was applied to segment MRI images of rat brain. The intercranial tissue of each rat was manually labeled. 476 rats (approximate 80%) were used for training set while 123 rats (approximate 20%) were used to test the performance of the trained U2-Net model. For evaluation, the segmentation result by the U2-Net model is compared with the manual label, and traditional segment methods. Quantitative evaluation, including Dice coefficient, Jaccard coefficient, Sensitivity, Specificity, Pixel accuracy, Hausdorff coefficient, True positive rate, False positive rate and the volumes of whole brain, were calculated to compare the segmentation results among different models.Main results.The U2-Net model was performed better than the software of RATS and BrainSuite, in which the quantitative values of training U2-Net model were 0.9907 ± 0.0016 (Dice coefficient), 0.9816 ± 0.0032 (Jaccard coefficient), 0.9912 ± 0.0020 (Sensitivity), 0.9989 ± 0.0002 (Specificity), 0.9982 ± 0.0003 (Pixel accuracy), 5.2390 ± 2.5334 (Hausdorff coefficient), 0.9902 ± 0.0025 (True positive rate), 0.0009 ± 0.0002(False positive rate) respectively.Significance.This study provides a new method that achieves reliable performance in rat brain skull stripping of MRI images, which could contribute to the processing of rat brain MRI.

Sleep deprivation aggravated amyloid ß oligomers-induced damage to the cerebellum of rats: Evidence from magnetic resonance imaging.

For quite a long time, researches on Alzheimer's disease (AD) primarily focused on the cortex and hippocampus, while the cerebellum has been ignored because of its abnormalities considered to appear in the late stage of AD. In recent years, increasing evidence suggest that the cerebellar pathological changes possibly occur in the preclinical phase of AD, which is also associated with sleep disorder. Sleep disturbance is a high risk factor of AD. However, the changes and roles of cerebellum has rarely been reported under conditions of AD accompanied with sleep disorders. In this study, using an amyloid-ß oligomers (AßO)-induced rat model of AD subjected to sleep deprivation, combining with a 7.0 T animals structural magnetic resonance imaging (MRI), we assessed structural changes of cerebellum in MRI. Our results showed that sleep deprivation combined with AßO led to an increased FA value in the anterior lobe of cerebellum, decreased ADC value in the cerebellar lobes and cerebellar nuclei, and increased cerebellum volume. Besides that, sleep deprivation exacerbated the damage of AßO to the cerebellar structural network. This study demonstrated that sleep deprivation could aggravate the damage to cerebellum induced by AßO. The present findings provide supporting evidence for the involvement of cerebellum in the early pathology of AD and sleep loss. Our data would contribute to advancing the understanding of the mysterious role of cerebellum in AD and sleep disorders, as well as would be helpful for developing non-invasive MRI biomarkers for screening early AD patients with self-reported sleep disturbances.

Association between gene expression and functional-metabolic architecture in Parkinson's disease.

Gene expression plays a critical role in the pathogenesis of Parkinson's disease (PD). How gene expression profiles are correlated with functional-metabolic architecture remains obscure. We enrolled 34 PD patients and 25 age-and-sex-matched healthy controls for simultaneous 18 F-FDG-PET/functional MRI scanning during resting state. We investigated the functional gradients and the ratio of standard uptake value. Principal component analysis was used to further combine the functional gradients and glucose metabolism into functional-metabolic architecture. Using partial least squares (PLS) regression, we introduced the transcriptomic data from the Allen Institute of Brain Sciences to identify gene expression patterns underlying the affected functional-metabolic architecture in PD. Between-group comparisons revealed significantly higher gradient variation in the visual, somatomotor, dorsal attention, frontoparietal, default mode, and subcortical network (pFDR < .048) in PD. Increased FDG-uptake was found in the somatomotor and ventral attention network while decreased FDG-uptake was found in the visual network (pFDR < .008). Spatial correlation analysis showed consistently affected patterns of functional gradients and metabolism (p = 2.47 × 10-8 ). PLS analysis and gene ontological analyses further revealed that genes were mainly enriched for metabolic, catabolic, cellular response to ions, and regulation of DNA transcription and RNA biosynthesis. In conclusion, our study provided genetic pathological mechanism to explain imaging-defined brain functional-metabolic architecture of PD.

Disrupted Topological Organization of Brain Network in Rats with Spatial Memory Impairments Induced by Acute Microwave Radiation.

Previous studies have suggested that microwave (MW) radiation with certain parameters can induce spatial memory deficits. However, the effect of MW on the topological organization of the brain network is still unknown. This work aimed to investigate the topological organization of the brain network in rats with spatial memory impairments induced by acute microwave (MW) radiation. The Morris water maze (MWM) test and resting-state functional magnetic resonance imaging were performed to estimate the spatial memory ability and brain network topological organization of the rats after MW exposure. Compared with the sham group, the rats exposed to 30 mW/cm2 1.5 GHz MW radiation exhibited a significantly decreased normalized clustering coefficient (γ) (p = 0.002) 1 d after the exposure and a prolonged average escape latency (AEL) (p = 0.014) 3 d after the exposure. Moreover, after 10 mW/cm2 1.5 GHz MW radiation, a significantly decreased γ (p = 0.003) was also observed in the rats, without any changes in AEL. In contrast, no adverse effects on AEL or topological parameters were observed after 9.375 GHz MW radiation. In conclusion, the rats with spatial memory deficits induced by MW radiation exhibited disruptions in the topological organization of the brain network. Moreover, these topological organization disruptions emerged earlier than behavioral symptom onset and could even be found in the rats without a decline in the performance of the spatial memory task. Therefore, it is possible to use the topological parameters of the brain network as early and sensitive indicators of the spatial memory impairments induced by acute MW radiation.

Overexpression of Sirt6 ameliorates sleep deprivation induced-cognitive impairment by modulating glutamatergic neuron function.

Sleep benefits the restoration of energy metabolism and thereby supports neuronal plasticity and cognitive behaviors. Sirt6 is a NAD+-dependent protein deacetylase that has been recognized as an essential regulator of energy metabolism because it modulates various transcriptional regulators and metabolic enzymes. The aim of this study was to investigate the influence of Sirt6 on cerebral function after chronic sleep deprivation (CSD). We assigned C57BL/6J mice to control or two CSD groups and subjected them to AAV2/9-CMV-EGFP or AAV2/9-CMV-Sirt6-EGFP infection in the prelimbic cortex (PrL). We then assessed cerebral functional connectivity (FC) using resting-state functional MRI, neuron/astrocyte metabolism using a metabolic kinetics analysis; dendritic spine densities using sparse-labeling; and miniature excitatory postsynaptic currents (mEPSCs) and action potential (AP) firing rates using whole-cell patch-clamp recordings. In addition, we evaluated cognition via a comprehensive set of behavioral tests. Compared with controls, Sirt6 was significantly decreased (P < 0.05) in the PrL after CSD, accompanied by cognitive deficits and decreased FC between the PrL and accumbens nucleus, piriform cortex, motor cortex, somatosensory cortex, olfactory tubercle, insular cortex, and cerebellum. Sirt6 overexpression reversed CSD-induced cognitive impairment and reduced FC. Our analysis of metabolic kinetics using [1-13C] glucose and [2-13C] acetate showed that CSD reduced neuronal Glu4 and GABA2 synthesis, which could be fully restored via forced Sirt6 expression. Furthermore, Sirt6 overexpression reversed CSD-induced decreases in AP firing rates as well as the frequency and amplitude of mEPSCs in PrL pyramidal neurons. These data indicate that Sirt6 can improve cognitive impairment after CSD by regulating the PrL-associated FC network, neuronal glucose metabolism, and glutamatergic neurotransmission. Thus, Sirt6 activation may have potential as a novel strategy for treating sleep disorder-related diseases.

IRE1α: from the function to the potential therapeutic target in atherosclerosis.

Inositol requiring enzyme 1 (IRE1) is generally thought to control the most conserved pathway in the unfolded protein response (UPR). Two isoforms of IRE1, IRE1α and IRE1ß, have been reported in mammals. IRE1α is a ubiquitously expressed protein whose knockout shows marked lethality. In contrast, the expression of IRE1ß is exclusively restricted in the epithelial cells of the respiratory and gastrointestinal tracts, and IRE1ß-knockout mice are phenotypically normal. As research continues to deepen, IRE1α was showed to be tightly linked to inflammation, lipid metabolism regulation, cell death and so on. Growing evidence also suggests an important role for IRE1α in promoting atherosclerosis (AS) progression and acute cardiovascular events through disrupting lipid metabolism balance, facilitating cells apoptosis, accelerating inflammatory responses and promoting foam cell formation. In addition, IRE1α was recognized as novel potential therapeutic target in AS prevention. This review provides some clues about the relationship between IRE1α and AS, hoping to contribute to further understanding roles of IRE1α in atherogenesis and to be helpful for the design of novel efficacious therapeutics agents targeting IRE1α-related pathways.

Altered Anterior Insular Metabolic Connectivity in Asymptomatic MAPT P301L Carriers.

BACKGROUND: The insula is the predominant brain region impaired in behavioral variant frontotemporal dementia (bvFTD). However, structural and functional changes in the sub-insula in the asymptomatic stage of bvFTD are unknown. OBJECTIVE: To describe structural and functional changes in insula subregions in asymptomatic carriers of the P301L mutation of the microtubule-associated protein tau (MAPT) gene and patients with bvFTD. METHODS: Six asymptomatic MAPT P301L mutation carriers and 12 MAPT negative control subjects of the same pedigree were enrolled, along with 30 patients with a clinical diagnosis of bvFTD and 30 matched controls. All subjects underwent hybrid positron emission tomography/magnetic resonance imaging. Atlas-based parcellation using a fine-grained Brainnetome Atlas was conducted to assess gray matter (GM) volume, metabolism, and metabolic connectivity in the sub-insula (region of interest). RESULTS: There was no significant GM atrophy or hypometabolism in insula subregions in asymptomatic MAPT P301L carriers, although decreased metabolic connectivity between vIa-middle temporal gyrus, vIa-temporal poles, dIa-middle temporal gyrus and dIa-temporal poles; and increased connectivity between vIa-orbitofrontal, vIa-dorsal lateral superior frontal gyrus, and dIa-orbitofrontal and dIa-dorsal lateral superior frontal gyrus were observed. Patients with bvFTD had significant atrophy and hypometabolism in all insula subregions and decreased metabolic connectivity in the whole brain, including vIa/dIa-middle temporal and vIa/dIa-temporal poles. The standardized uptake value ratios of vIa and dIa were negatively associated with Frontal behavior inventory disinhibition scale scores. CONCLUSION: Metabolic connectivity is altered in vIa and dIa subregions of the sub-insula in MAPT P301L mutation carriers before the occurrence of atrophy, hypometabolism, and clinical symptoms.

Metabolic Asymmetry Relates to Clinical Characteristics and Brain Network Abnormalities in Alzheimer's Disease.

BACKGROUND: Metabolic asymmetry has been observed in Alzheimer's disease (AD), but different studies have inconsistent viewpoints. OBJECTIVE: To analyze the asymmetry of cerebral glucose metabolism in AD and investigate its clinical significance and potential metabolic network abnormalities. METHODS: Standardized uptake value ratios (SUVRs) were obtained from 18F-FDG positron emission tomography (PET) images of all participants, and the asymmetry indices (AIs) were calculated according to the SUVRs. AD group was divided into left/right-dominant or bilateral symmetric hypometabolism (AD-L/AD-R or AD-BI) when more than half of the AIs of the 20 regions of interest (ROIs) were < -2SD, >2SD, or between±1SD. Differences in clinical features among the three AD groups were compared, and the abnormal network characteristics underlying metabolic asymmetry were explored. RESULTS: In AD group, the proportions of AD-L, AD-R, and AD-BI were 28.4%, 17.9%, and 18.5%, respectively. AD-L/AD-R groups had younger age of onset and faster rate of cognitive decline than AD-BI group (p < 0.05). The absolute values of AIs in half of the 20 ROIs became higher at follow-up than at baseline (p < 0.05). Compared with those in AD-BI group, metabolic connection strength of network, global efficiency, cluster coefficient, degree centrality and local efficiency were lower, but shortest path length was longer in AD-L and AD-R groups (p < 0.05). CONCLUSION: Asymmetric and symmetric hypometabolism may represent different clinical subtypes of AD, which may provide a clue for future studies on the heterogeneity of AD and help to optimize the design of clinical trials.

Correlation of abnormal brain changes with perinatal factors in very preterm infants based on diffusion tensor imaging.

Background: It remains unclear whether very preterm (VP) infants have the same level of brain structure and function as full-term (FT) infants. In addition, the relationship between potential differences in brain white matter microstructure and network connectivity and specific perinatal factors has not been well characterized. Objective: This study aimed to investigate the existence of potential differences in brain white matter microstructure and network connectivity between VP and FT infants at term-equivalent age (TEA) and examine the potential association of these differences with perinatal factors. Methods: A total of 83 infants were prospectively selected for this study: 43 VP infants (gestational age, or GA: 27-32 weeks) and 40 FT infants (GA: 37-44 weeks). All infants at TEA underwent both conventional magnetic resonance imaging (MRI) and diffusion tensor imaging (DTI). Significant differences in white matter fractional anisotropy (FA) and mean diffusivity (MD) images between the VP and FT groups were observed using tract-based spatial statistics (TBSS). The fibers were tracked between each pair of regions in the individual space, using the automated anatomical labeling (AAL) atlas. Then, a structural brain network was constructed, where the connection between each pair of nodes was defined by the number of fibers. Network-based statistics (NBS) were used to examine differences in brain network connectivity between the VP and FT groups. Additionally, multivariate linear regression was conducted to investigate potential correlations between fiber bundle numbers and network metrics (global efficiency, local efficiency, and small-worldness) and perinatal factors. Results: Significant differences in FA were observed between the VP and FT groups in several regions. These differences were found to be significantly associated with perinatal factors such as bronchopulmonary dysplasia (BPD), activity, pulse, grimace, appearance, respiratory (APGAR) score, gestational hypertension, and infection. Significant differences in network connectivity were observed between the VP and FT groups. Linear regression results showed significant correlations between maternal years of education, weight, the APGAR score, GA at birth, and network metrics in the VP group. Conclusions: The findings of this study shed light on the influence of perinatal factors on brain development in VP infants. These results may serve as a basis for clinical intervention and treatment to improve the outcome of preterm infants.

Multiparametric Magnetic Resonance Imaging With Comprehensive Assessment of Prostate Volume, Morphology, and Composition Better Reflects the Correlation With International Prostate Symptom Score.

OBJECTIVE: To investigate the application of multiparametric magnetic resonance imaging (mp-MRI) for comprehensive evaluation of the correlation between the characteristics of the transitional zone and the International Prostate Symptom Score (IPSS) in patients with benign prostatic hyperplasia (BPH). MATERIALS AND METHODS: We retrospectively recruited 210 patients with biopsy-proven BPH who underwent preoperative mp-MRI and were assigned an IPSS. The evaluation indicators included prostate volumetric parameters (total prostate volume [TPV], transition zone volume [TZV], and transition zone index [TZI, TZI=TZV/TPV]), prostate morphological parameters (intravesical prostatic protrusion, and presumed circle area ratio) and prostate compositional parameters (apparent diffusion coefficient [ADC], and mean signal intensity of T2WI [mean-SI-T2WI]). The Pearson (r) correlation coefficient, one-way analysis of variance, and multiple linear regression analysis were used to build a regression model for evaluating the correlation between MRI-derived parameters and IPSS, IPSS-storage symptom, IPSS-voiding symptom. RESULTS: Significant correlations were found between IPSS, IPSS-storage symptom, IPSS-voiding symptom, and prostate MRI-derived parameters, including TPV (r = 0.350; r = 0.466; r = 0.225, P < .001), TZV (r = 0.374; r = 0.492; r = 0.243, P < .001), TZI (r = 0.383; r = 0.313; r = 0.354, P < .001), presumed circle area ratio (r = 0.481; r = 0.356; r = 0.469, P < .001), ADC(r = -0.198; r = -0.053; r = -0.239, P < .05) and mean-SI-T2WI (r = -0.626; r = -0.310; r = -0.687, P < .001), respectively. Based on multiple linear regression analysis, the impact of mean-SI-T2WI and TZI on total IPSS were statistically significant (P < .05), and the regression equation established with the analysis (IPSS= 39.224 + 8.469 ×TZI+ (-0.09)× (mean-SI-T2WI)) was statistically significant (F=104.995, P < .001). CONCLUSION: Mp-MRI could be used to evaluate the volume and morphology of BPH. In particular, mean-SI-T2WI and ADC could be used to describe the internal composition of the prostate. The imaging parameters were effective for evaluating BPH.

Involvement of specific striatal subregion contributes to executive deficits in Alzheimer disease.

BACKGROUND: There is growing evidence that the striatum plays a central role in cognitive dysfunction. However, it remains unclear whether and how the striatum contributes specifically to executive deficits in Alzheimer disease (AD). We sought to elucidate aberrations in the striatal subregion associated with executive function and its metabolic connectivity with the cortical regions to investigate its role in the pathogenesis of executive deficits in patients with AD. METHODS: Patients with AD and healthy controls underwent a neuropsychological assessment battery, including assessment of executive function, and a hybrid positron emission tomography/magnetic resonance imaging (PET/MRI) scan. We performed voxel-wise analyses of cerebral metabolism between patients and controls, focusing on the executive subregion of the striatum according to the Oxford-GSK-Imanova Striatal Connectivity Atlas. We assessed the correlation between the [18F]-fluorodeoxyglucose standardized uptake value ratio of the striatal executive subregion and clinical variables, and we analyzed seed-based metabolic connectivity of the striatal executive subregion with the dorsolateral prefrontal cortex (DLPFC) using [18F]-fluorodeoxyglucose PET. RESULTS: We included 50 patients with AD and 33 controls in our analyses. The patterns of striatal hypometabolism in patients with AD were specific to executive and caudal motor subregions. Metabolic activity in the executive subregion of the striatum correlated negatively with the severity of executive dysfunction, as measured with the Trial-Making Test (TMT) part B and the difference score TMT B-A, and correlated positively with Digit Span (backward) and Verbal Fluency Test scales, particularly on the left side. Compared with controls, patients with AD showed reduced metabolic connectivity between striatal executive subregions and the dorsolateral prefrontal cortex (DLPFC). LIMITATIONS: Our study was limited by small sample sizes and cross-sectional findings. CONCLUSION: Our findings show that patients with AD have impairments in the executive subregion of the striatum, and these deficits may be associated with a disconnection between the executive striatum and DLPFC, providing valuable insight into the pathogenesis of this disease.