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Purpose To assess the brain core temperature of Alzheimer disease (AD) patients in comparison with healthy volunteers using diffusion-weighted thermometry. Materials and methods Fourteen AD patients (3 men, 11 women; age range 60–81 years, mean age 73.8 ± 6.1 years) and 14 healthy volunteers, age and sex-matched (mean age 70.1 ± 6.9 years; range 62–84 years; 5 men, 9 women) underwent MR examination between February 2014 and March 2016. MR imaging studies were performed with a 1.5-T MR scanner. Brain core temperature ( T : °C) was calculated using the following equation from the diffusion coefficient ( D ) in the lateral ventricular (LV) cerebrospinal fluid: T  = 2256.74/ln (4.39221/ D ) − 273.15 using a standard DWI single-shot echo-planar pulse sequence ( b value 1000 s/mm 2 ). Statistical analysis was performed using a nonparametric Wilcoxon rank-sum test to compare the patient and control groups regarding LV temperatures. Results There was no significant difference ( P  = 0.1937) in LV temperature between patients (mean 37.9 ± 1.1 °C, range 35.8–39.2 °C) and control group (38.7 ± 1.4 °C, range 36.9–42.7 °C). Conclusions Brain core temperature in AD patients showed no significant alterations compared to healthy volunteers.

The location of an acute ischemic stroke is associated with its prognosis. The widely used Gaussian model-based parameter, apparent diffusion coefficient (ADC), cannot reveal microstructural changes in different locations or the degree of infarction. This prospective observational study was reviewed and approved by the Institutional Review Board of Xiamen Second Hospital, China (approval No. 2014002).Diffusion kurtosis imaging (DKI) was used to detect 199 lesions in 156 patients with acute ischemic stroke (61 males and 95 females), mean age 63.15 ± 12.34 years. A total of 199 lesions were located in the periventricular white matter (n = 52), corpus callosum (n = 14), cerebellum (n = 29), basal ganglia and thalamus (n = 21), brainstem (n = 21) and gray-white matter junctions (n = 62). Percentage changes of apparent diffusion coefficient (ΔADC) and DKI-derived indices (fractional anisotropy [ΔFA], mean diffusivity [ΔMD], axial diffusivity [ΔDa], radial diffusivity ΔDr, mean kurtosis [ΔMK], axial kurtosis [ΔKa], and radial kurtosis [ΔKr]) of each lesion were computed relative to the normal contralateral region. The results showed that (1) there was no significant difference in ΔADC, ΔMD, ΔDa or ΔDr among almost all locations. (2) There was significant difference in ΔMK among almost all locations (except basal ganglia and thalamus vs. brain stem; basal ganglia and thalamus vs. gray-white matter junctions; and brainstem vs. gray-white matter junctions. (3) The degree of change in diffusional kurtosis in descending order was as follows: corpus callosum > periventricular white matter > brainstem > gray-white matter junctions > basal ganglia and thalamus > cerebellum. In conclusion, DKI could reveal the differences in microstructure changes among various locations affected by acute ischemic stroke, and performed better than diffusivity among all groups.

Neurodevelopmental disorders (NDDs) can severely impact functioning yet effective treatments are limited. Greater insight into the neurobiology underlying NDDs is critical to the development of successful treatments. Using a genetics‐first approach, we investigated the potential of advanced diffusion‐weighted imaging (DWI) techniques to characterize the neural microstructure unique to neurofibromatosis type 1 (NF1) and Noonan syndrome (NS). In this prospective study, children with NF1, NS, and typical developing (TD) were scanned using a multi‐shell DWI sequence optimized for neurite orientation density and dispersion imaging (NODDI) and diffusion kurtosis imaging (DKI). Region‐of‐interest and tract‐based analysis were conducted on subcortical regions and white matter tracts. Analysis of covariance, principal components, and linear discriminant analysis compared between three groups. 88 participants (Mage = 9.36, SDage = 2.61; 44 male) were included: 31 NS, 25 NF1, and 32 TD. Subcortical regions differed between NF1 and NS, particularly in the thalamus where the neurite density index (NDI; estimated difference 0.044 [95% CI: −0.034, 0.053], d = 2.36), orientation dispersion index (ODI; estimate 0.018 [95% CI: 0.010, 0.026], d = 1.39), and mean kurtosis (MK; estimate 0.049 [95% CI: 0.025, 0.072], d = 1.39) were lower in NF1 compared with NS (all p < 0.0001). Reduced NDI was found in NF1 and NS compared with TD in all 39 white matter tracts investigated (p < 0.0001). Reduced MK was found in a majority of the tracts in NF1 and NS relative to TD, while fewer differences in ODI were observed. The middle cerebellar peduncle showed lower NDI (estimate 0.038 [95% CI: 0.021, 0.056], p < 0.0001) and MK (estimate 0.057 [95% CI: 0.026, 0.089], p < 0.0001) in NF1 compared to NS. Multivariate analyses distinguished between groups using NDI, ODI, and MK measures. Principal components analysis confirmed that the clinical groups differ most from TD in white matter tract‐based NDI and MK, whereas ODI values appear similar across the groups. The subcortical regions showed several differences between NF1 and NS, to the extent that a linear discriminant analysis could classify participants with NF1 with an accuracy rate of 97%. Differences in neural microstructure were detected between NF1 and NS, particularly in subcortical regions and the middle cerebellar peduncle, in line with pre‐clinical evidence. Advanced DWI techniques detected subtle alterations not found in prior work using conventional diffusion tensor imaging. Differences in brain microstructure between neurodevelopmental disorders neurofibromatosis type‐1 (NF1) and Noonan syndrome (NS)were detected using neurite orientation density and dispersion imaging and diffusion‐kurtosis imaging. Differential decreases in neurite density (NDI) and mean kurtosis (MK) were found in each condition compared to age and sex matched typically developing (TD), particularly in the middle cerebellar peduncle.

Structural deficits in white matter fibre have been linked to psychosis. However, it remains unclear whether these aberrations are present in individuals that experience non‐clinical psychotic‐like experiences, predating illness onset. While previous research demonstrates that alterations in white matter in schizotypy are consistent with those in clinical psychosis, these studies often dichotomise healthy samples into high and low schizotypy, which may reduce statistical sensitivity. Previous research is also confounded by the investigation of diffusion MRI parameters that fail to account for complex crossing fibre populations. In this work, we treat psychotic‐like experiences as a continuous variable, and applied Fixel‐Based Analysis (FBA), a framework for investigating microstructural and morphological effects in brain white matter using diffusion‐weighted imaging data. Across two independent cohorts of healthy participants with varied psychotic‐like experiences including data from the IMAGEN consortium (Study 1 n = 41; Study 2 n = 1098), we hypothesized that greater psychotic‐like experiences would be associated with FBA metrics sensitive to microstructural fibre density and/or cross‐sectional morphological effects. Contrary to our hypothesis, we did not find significant correlations between psychotic‐like experiences and FBA metrics across either dataset (FWE p < 0.05). Bayesian analysis of tract‐aggregated data showed substantial evidence of no association (Bayes factor < 1/3) between psychotic‐like experiences and fibre density, nor cross‐sectional morphology, across several white matter tracts of interest, pre‐defined from prior neuroimaging literature. These findings suggest that the relationship between non‐clinical psychotic‐like experiences and white matter microstructure may not be as robust as previously thought. This raises the possibility that white matter alterations across the psychosis spectrum echo clinical diagnostic thresholding, with observable effects in clinical but not sub‐clinical presentations. Our findings show no association between whole‐brain fibre‐specific properties of white matter microstructure and sub‐clinical psychotic‐like experiences. Further, we show evidence for the lack of an association within tract‐aggregated fibre‐specific metrics. Future research should integrate longitudinal designs to explore whether fibre‐specific white matter attributes provide clinically meaningful insight into the risk of psychosis onset. We used Fixel‐Based Analysis (FBA) to investigate the relationship between psychotic‐like experiences and white matter microstructure across two independent cohorts of healthy participants (Study 1: n = 41; Study 2: n = 1098). Contrary to our hypothesis, we found no significant correlation between FBA metrics of white matter microstructure and psychotic‐like experiences.

Tractography is widely used in human studies of connectivity with respect to every brain region, function, and is explored developmentally, in adulthood, ageing, and in disease. However, the core issue of how to systematically threshold, taking into account the inherent differences in connectivity values for different track lengths, and to do this in a comparable way across studies has not been solved. By utilising 54 healthy individuals' diffusion‐weighted image data taken from HCP, this study adopted Monte Carlo derived distance‐dependent distributions (DDDs) to generate distance‐dependent thresholds with various levels of alpha for connections of varying lengths. As a test case, we applied the DDD approach to generate a language connectome. The resulting connectome showed both short‐ and long‐distance structural connectivity in the close and distant regions as expected for the dorsal and ventral language pathways, consistent with the literature. The finding demonstrates that the DDD approach is feasible to generate data‐driven DDDs for common thresholding and can be used for both individual and group thresholding. Critically, it offers a standard method that can be applied to various probabilistic tracking datasets. The resulting connectome showed expected short‐ and long‐distance structural connectivity in the close and distant regions for the dorsal and ventral language pathways, consistent with the literature.

Background and Purpose The role of asymptomatic diffusion‐weighted imaging‐positive (aDWI+) lesions in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) patients remains unclear, and their radiographic features may differ from those of symptomatic diffusion‐weighted imaging‐positive (sDWI+) lesions. We aimed to investigate the clinicoradiographic characteristics of aDWI+ lesions in CADASIL patients. Methods We conducted a retrospective analysis using data from the Taiwan CADASIL Registry. aDWI+ lesions were defined as incidentally detected DWI+ lesions without corresponding acute neurological deficits. We compared the baseline clinical characteristics of patients with and without aDWI+ lesions and analyzed their radiological features and evolution in relation to sDWI+ lesions. Results Among 154 enrolled patients (mean age 62 ± 10 years), 17 (11%) had aDWI+ lesions. Baseline clinical characteristics were similar in the two groups, but those with aDWI+ lesions had more lacunes (median 8 vs. 2), multiple cerebral microbleeds (CMBs; 85% vs. 40%), and anterior temporal white matter hyperintensity (WMH; 47% vs. 14%). Multivariable analysis showed that aDWI+ lesions were associated with anterior temporal WMH (odds ratio 5.7, 95% confidence interval 1.5–21.0) after adjusting for multiple lacunes, multiple CMBs, and total WMH score. Compared to sDWI+ lesions, aDWI+ lesions were more often small infarcts (<1 cm; 89% vs. 23%) and less likely to involve the corticospinal tract (11% vs. 96%). Among the 11 aDWI+ lesions with follow‐up magnetic resonance imaging, seven became microinfarcts, three became lacunes, and one disappeared. Conclusions aDWI+ lesions in CADASIL are not uncommon and are associated with higher burdens of small vessel disease and anterior temporal WMH. Further research is needed to assess their long‐term impact on CADASIL.

Accelerated maturation of brain parenchyma close to term‐equivalent age leads to rapid changes in diffusion‐weighted imaging (DWI) and diffusion tensor imaging (DTI) metrics of neonatal brains, which can complicate the evaluation and interpretation of these scans. In this study, we characterized the topography of age‐related evolution of diffusion metrics in neonatal brains. We included 565 neonates who had MRI between 0 and 3 months of age, with no structural or signal abnormality—including 162 who had DTI scans. We analyzed the age‐related changes of apparent diffusion coefficient (ADC) values throughout brain and DTI metrics (fractional anisotropy [FA] and mean diffusivity [MD]) along white matter (WM) tracts. Rate of change in ADC, FA, and MD values across 5 mm cubic voxels was calculated. There was significant reduction of ADC and MD values and increase of FA with increasing gestational age (GA) throughout neonates' brain, with the highest temporal rates in subcortical WM, corticospinal tract, cerebellar WM, and vermis. GA at birth had significant effect on ADC values in convexity cortex and corpus callosum as well as FA/MD values in corpus callosum, after correcting for GA at scan. We developed online interactive atlases depicting age‐specific normative values of ADC (ages 34–46 weeks), and FA/MD (35–41 weeks). Our results show a rapid decrease in diffusivity metrics of cerebral/cerebellar WM and vermis in the first few weeks of neonatal age, likely attributable to myelination. In addition, prematurity and low GA at birth may result in lasting delay in corpus callosum myelination and cerebral cortex cellularity. In this study, we characterized the topography of age‐related evolution of diffusion metrics in neonatal brains. In addition, we developed online interactive atlases depicting age‐specific normative values of apparent diffusion coefficient, fractional anisotropy, and mean diffusivity.

Rich‐club organization is key to efficient global neuronal signaling and integration of information. Alterations interfere with higher‐order cognitive processes, and are common to several psychiatric and neurological conditions. A few studies examining the structural connectome in obsessive–compulsive disorder (OCD) suggest lower efficiency of information transfer across the brain. However, it remains unclear whether this is due to alterations in rich‐club organization. In the current study, the structural connectome of 28 unmedicated OCD patients, 8 of their unaffected siblings and 28 healthy controls was reconstructed by means of diffusion‐weighted imaging and probabilistic tractography. Topological and weighted measures of rich‐club organization and connectivity were computed, alongside global and nodal measures of network integration and segregation. The relationship between clinical scores and network properties was explored. Compared to healthy controls, OCD patients displayed significantly lower topological and weighted rich‐club organization, allocating a smaller fraction of all connection weights to the rich‐club core. Global clustering coefficient, local efficiency, and clustering of nonrich club nodes were significantly higher in OCD patients. Significant three‐group differences emerged, with siblings displaying highest and lowest values in different measures. No significant correlation with any clinical score was found. Our results suggest weaker structural connectivity between rich‐club nodes in OCD patients, possibly resulting in lower network integration in favor of higher network segregation. We highlight the need of looking at network‐based alterations in brain organization and function when investigating the neurobiological basis of this disorder, and stimulate further research into potential familial protective factors against the development of OCD. The present study investigates rich‐club organization and rich‐club connectivity as potential markers of OCD, by using probabilistic tractography to reconstruct the white‐matter network of a group of unmedicated OCD patients. Our results suggest weaker structural connectivity between rich‐club nodes in OCD patients, possibly resulting in lower network integration in favor of higher network segregation.

INTRODUCTION Whether Alzheimer's disease pathology involves white matter pathways connecting the locus coeruleus (LC) to the entorhinal cortex (EC) is unclear. In this cross‐sectional observational study, we investigated the microstructural integrity of the LC–EC pathway in relation to amyloid, tau, and neurodegeneration (ATN) biomarkers along the cognitive spectrum from normal cognition to dementia. METHODS One hundred twenty‐four participants underwent clinical assessment, diffusion‐weighted imaging, structural magnetic resonance imaging (N), amyloid (A), and tau (T) positron emission tomography. Diffusivity indices were assessed in the LC–EC tract using a probabilistic atlas, and linear models were used to assess associations with ATN markers and cognition. RESULTS Differences in LC–EC microstructural parameters were observed in participants with Braak stage > I versus Braak 0 (p < 0.020), N+ versus N− (p < 0.001), and cognitively impaired versus unimpaired (p < 0.019). LC–EC mean diffusivity was associated with Mini‐Mental State Examination score even after accounting for ATN markers (p = 0.015). DISCUSSION Our results suggest that LC–EC diffusivity provides complementary information over ATN biomarkers in explaining cognitive impairment. Highlights Locus coeruleus–entorhinal cortex (LC–EC) tract microstructure is associated with tau and especially neurodegeneration markers. LC–EC tract microstructure is more sensitive to tau pathology and neurodegeneration than tracts commonly affected in Alzheimer's disease. LC–EC diffusivity measures provide complementary information over amyloid, tau, and neurodegeneration (ATN) biomarkers.

Some in vitro experiments have shown that erythropoietin （EPO） increases resistance to apoptosis and facilitates neuronal survival follow- ing cerebral ischemia. However, results from in vivo studies are rarely reported. Perfusion-weighted imaging （PWI） and diffusion-weighted imaging （DWI） have been applied successfully to distinguish acute cerebral ischemic necrosis and penumbra in living animals; therefore, we hypothesized that PWI and DWI could be used to provide imaging evidence in vivo for the conclusion that EPO could reduce apoptosis in brain areas injured by cerebral ischemia/reperfusion. To validate this hypothesis, we established a rat model of focal cerebral ischemia/ reperfusion injury, and treated with intra-cerebroventricular injection of EPO （5,000 U/kg） 20 minutes before injury. Brain tissue in the ischemic injury zone was sampled using MRI-guided localization. The relative area of abnormal tissue, changes in PWI and DWI in the ischemic injury zone, and the number of apoptotic cells based on TdT-mediated dUTP-biotin nick end-labeling （TUNEL） were assessed. Our findings demonstrate that EPO reduces the relative area of abnormally high signal in PWI and DWI, increases cerebral blood volume, and decreases the number of apoptotic cells positive for TUNEL in the area injured by cerebral ischemia/reperfusion. The experiment pro- vides imaging evidence in vivo for EPO treating cerebral ischemia/reperfusion injury.