Decomposition of an odorant in olfactory perception and neural representation.

Molecules-the elementary units of substances-are commonly considered the units of processing in olfactory perception, giving rise to undifferentiated odour objects invariant to environmental variations. By selectively perturbing the processing of chemical substructures with adaptation ('the psychologist's microelectrode') in a series of psychophysical and neuroimaging experiments (458 participants), we show that two perceptually distinct odorants sharing part of their structural features become significantly less discernible following adaptation to a third odorant containing their non-shared structural features, in manners independent of olfactory intensity, valence, quality or general olfactory adaptation. The effect is accompanied by reorganizations of ensemble activity patterns in the posterior piriform cortex that parallel subjective odour quality changes, in addition to substructure-based neural adaptations in the anterior piriform cortex and amygdala. Central representations of odour quality and the perceptual outcome thus embed submolecular structural information and are malleable by recent olfactory encounters.

H-ferritin-nanocaged gadolinium nanoparticles for ultra-sensitive MR molecular imaging.

Rationale: Magnetic resonance imaging (MRI) is a powerful diagnostic technology by providing high-resolution imaging. Although MRI is sufficiently valued in its resolving morphology, it has poor sensitivity for tracking biomarkers. Therefore, contrast agents are often used to improve MRI diagnostic sensitivity. However, the clinically used Gd chelates are limited in improving MRI sensitivity owing to their low relaxivity. The objective of this study is to develop a novel contrast agent to achieve a highly sensitive tracking of biomarkers in vivo. Methods: A Gd-based nanoprobe composed of a gadolinium nanoparticle encapsulated within a human H-ferritin nanocage (Gd-HFn) has been developed. The specificity and sensitivity of Gd-HFn were evaluated in vivo in tumor-bearing mice and apolipoprotein E-deficient mice (Apoe-/-) by MRI. Results: The Gd-HFn probe shows extremely high relaxivity values (r1 = 549 s-1mM-1, r2 = 1555 s-1mM-1 under a 1.5-T magnetic field; and r1 = 428 s-1mM-1 and r2 = 1286 s-1mM-1 under a 3.0-T magnetic field), which is 175-fold higher than that of the clinically standard Dotarem (Gd-DOTA, r1 =3.13 s-1mM-1) under a 1.5-T magnetic field, and 150-fold higher under a 3.0-T magnetic field. Owing to the substantially enhanced relaxivity values, Gd-HFn achieved a highly sensitive tracking for the tumor targeting receptor of TfR1 and enabled the in vivo MRI visualization of tumors approaching the angiogenic switch. Conclusions: The developed Gd-HFn contrast agent makes MRI a more powerful tool by simultaneously providing functional and morphological imaging information, which paves the way for a new perspective in molecular imaging.

Neural representation of gestalt grouping and attention effect in human visual cortex.

BACKGROUND: The brain aggregates meaningless local sensory elements to form meaningful global patterns in a process called perceptual grouping. Current brain imaging studies have found that neural activities in V1 are modulated during visual grouping. However, how grouping is represented in each of the early visual areas, and how attention alters these representations, is still unknown. NEW METHOD: We adopted MVPA to decode the specific content of perceptual grouping by comparing neural activity patterns between gratings and dot lattice stimuli which can be grouped with proximity law. Furthermore, we quantified the grouping effect by defining the strength of grouping, and assessed the effect of attention on grouping. RESULTS: We found that activity patterns to proximity grouped stimuli in early visual areas resemble these to grating stimuli with the same orientations. This similarity exists even when there is no attention focused on the stimuli. The results also showed a progressive increase of representational strength of grouping from V1 to V3, and attention modulation to grouping is only significant in V3 among all the visual areas. COMPARISON WITH EXISTING METHODS: Most of the previous work on perceptual grouping has focused on how activity amplitudes are modulated by grouping. Using MVPA, the present work successfully decoded the contents of neural activity patterns corresponding to proximity grouping stimuli, thus shed light on the availability of content-decoding approach in the research on perceptual grouping. CONCLUSIONS: Our work found that the content of the neural activity patterns during perceptual grouping can be decoded in the early visual areas under both attended and unattended task, and provide novel evidence that there is a cascade processing for proximity grouping through V1 to V3. The strength of grouping was larger in V3 than in any other visual areas, and the attention modulation to the strength of grouping was only significant in V3 among all the visual areas, implying that V3 plays an important role in proximity grouping.

Differential effects of social isolation on oligodendrocyte development in different brain regions: insights from a canine model.

Social isolation (SI) exerts diverse adverse effects on brain structure and function in humans. To gain an insight into the mechanisms underlying these effects, we conducted a systematic analysis of multiple brain regions from socially isolated and group-housed dogs, whose brain and behavior are similar to humans. Our transcriptomic analysis revealed reduced expression of myelin-related genes specifically in the white matter of prefrontal cortex (PFC) after SI during the juvenile stage. Despite these gene expression changes, myelin fiber organization in PFC remained unchanged. Surprisingly, we observed more mature oligodendrocytes and thicker myelin bundles in the somatosensory parietal cortex in socially isolated dogs, which may be linked to an increased expression of ADORA2A, a gene known to promote oligodendrocyte maturation. Additionally, we found a reduced expression of blood-brain barrier (BBB) structural components Aquaporin-4, Occludin, and Claudin1 in both PFC and parietal cortices, indicating BBB disruption after SI. In agreement with BBB disruption, myelin-related sphingolipids were increased in cerebrospinal fluid in the socially isolated group. These unexpected findings show that SI induces distinct alterations in oligodendrocyte development and shared disruption in BBB integrity in different cortices, demonstrating the value of dogs as a complementary animal model to uncover molecular mechanisms underlying SI-induced brain dysfunction.

Visual number sense for real-world scenes shared by deep neural networks and humans.

Recently, visual number sense has been identified from deep neural networks (DNNs). However, whether DNNs have the same capacity for real-world scenes, rather than the simple geometric figures that are often tested, is unclear. In this study, we explore the number perception of scenes using AlexNet and find that numerosity can be represented by the pattern of group activation of the category layer units. The global activation of these units increases with the number of objects in the scene, and the variations in their activation decrease accordingly. By decoding the numerosity from this pattern, we reveal that the embedding coefficient of a scene determines the likelihood of potential objects to contribute to numerical perception. This was demonstrated by the more optimized performance for pictures with relatively high embedding coefficients in both DNNs and humans. This study for the first time shows that a distinct feature in visual environments, revealed by DNNs, can modulate human perception, supported by a group-coding mechanism.

Leading basic modes of spontaneous activity drive individual functional connectivity organization in the resting human brain.

Spontaneous activity of the human brain provides a window to explore intrinsic principles of functional organization. However, most studies have focused on interregional functional connectivity. The principles underlying rich repertoires of instantaneous activity remain largely unknown. We apply a recently proposed eigen-microstate analysis to three resting-state functional MRI datasets to identify basic modes that represent fundamental activity patterns that coexist over time. We identify five leading basic modes that dominate activity fluctuations. Each mode exhibits a distinct functional system-dependent coactivation pattern and corresponds to specific cognitive profiles. In particular, the spatial pattern of the first leading basis mode shows the separation of activity between the default-mode and primary and attention regions. Based on theoretical modelling, we further reconstruct individual functional connectivity as the weighted superposition of coactivation patterns corresponding to these leading basic modes. Moreover, these leading basic modes capture sleep deprivation-induced changes in brain activity and interregional connectivity, primarily involving the default-mode and task-positive regions. Our findings reveal a dominant set of basic modes of spontaneous activity that reflect multiplexed interregional coordination and drive conventional functional connectivity, furthering the understanding of the functional significance of spontaneous brain activity.

Excitatory-inhibitory modulation of transcranial focus ultrasound stimulation on human motor cortex.

AIMS: Transcranial focus ultrasound stimulation (tFUS) is a promising non-invasive neuromodulation technology. This study aimed to evaluate the modulatory effects of tFUS on human motor cortex (M1) excitability and explore the mechanism of neurotransmitter-related intracortical circuitry and plasticity. METHODS: Single pulse transcranial magnetic stimulation (TMS)-eliciting motor-evoked potentials (MEPs) were used to assessed M1 excitability in 10 subjects. Paired-pulse TMS was used to measure the effects of tFUS on GABA- and glutamate-related intracortical excitability and 1 H-MRS was used to assess the effects of repetitive tFUS on GABA and Glx (glutamine + glutamate) neurometabolic concentrations in the targeting region in nine subjects. RESULTS: The etFUS significantly increased M1 excitability, decreased short interval intracortical inhibition (SICI) and long interval intracortical inhibition (LICI). The itFUS significantly suppressed M1 excitability, increased SICI, LICI, and decreased intracortical facilitation (ICF). Seven times of etFUS decreased the GABA concentration (6.32%), increased the Glx concentration (12.40%), and decreased the GABA/Glx ratio measured by MRS, while itFUS increased the GABA concentration (18.59%), decreased Glx concentration (0.35%), and significantly increased GABA/Glx ratio. CONCLUSION: The findings support that tFUS with different parameters can exert excitatory and inhibitory neuromodulatory effects on the human motor cortex. We provide novel insights that tFUS change cortical excitability and plasticity by regulating excitatory-inhibition balance related to the GABAergic and glutamatergic receptor function and neurotransmitter metabolic level.

Multidelay MR Arterial Spin Labeling Perfusion Map for the Prediction of Cerebral Hyperperfusion After Carotid Endarterectomy.

BACKGROUND: Multidelay arterial spin labeling (ASL) generates time-resolved perfusion maps, which may provide sufficient and accurate hemodynamic information in carotid stenosis. PURPOSE: To use imaging markers derived from multidelay ASL magnetic resonance imaging (MRI) and to determine the optimal strategy for predicting cerebral hyperperfusion after carotid endarterectomy (CEA). STUDY TYPE: Prospective observational cohort. SUBJECTS: A total of 79 patients who underwent CEA for carotid stenosis. FIELD STRENGTH/SEQUENCE: A 3.0 T/pseudo-continuous ASL with three postlabeling delays of 1.0, 1.57, and 2.46 seconds using fast-spin echo readout. ASSESSMENT: Cerebral perfusion pressure, antegrade, and collateral flow were scored on a four-grade ordinal scale based on preoperative multidelay ASL perfusion maps. Simultaneously, quantitative hemodynamic parameters including cerebral blood flow (CBF), arterial transit time (ATT), relative CBF (rCBF) and relative ATT (rATT; ipsilateral/contralateral values) were calculated. On the CBF ratio map obtained through dividing postoperative by preoperative CBF map, regions of interest were placed covering ipsilateral middle cerebral artery territory. Three neuroradiologists conducted this procedure. Cerebral hyperperfusion was defined as a CBF ratio >2. STATISTICAL TESTS: Weighted κ values, independent sample t test, chi-square test, Mann-Whitney U-test, multivariable logistic regression analysis, receiver-operating characteristic curve analysis, and Delong test. Significance level was P < 0.05. RESULTS: Cerebral hyperperfusion was observed in 15 (19%) patients. Higher blood pressure (odd ratio [OR] = 1.08) and carotid near-occlusion (NO; OR = 7.31) were clinical risk factors for postoperative hyperperfusion. Poor ASL perfusion score (OR = 37.33), decreased CBF (OR = 0.74), prolonged ATT (OR = 1.02), lower rCBF (OR = 0.91), and higher rATT (OR = 1.12) were independent imaging predictors of hyperperfusion. ASL perfusion score exhibited the highest specificity (95.3%), while CBF exhibited the highest sensitivity (93.3%) for the prediction of hyperperfusion. When combined with ASL perfusion score, CBF and ATT, the predictive ability was significantly higher than using blood pressure and NO alone (AUC: 0.98 vs. 0.78). DATA CONCLUSIONS: Multidelay ASL can accurately predict cerebral hyperperfusion after CEA with high sensitivity and specificity. EVIDENCE LEVEL: 2 TECHNICAL EFFICACY: Stage 5.

Neuroanatomical Localization of Rapid Eye Movement Sleep Behavior Disorder in Human Brain Using Lesion Network Mapping.

OBJECTIVE: To localize the neuroanatomical substrate of rapid eye movement sleep behavior disorder (RBD) and to investigate the neuroanatomical locational relationship between RBD and α-synucleinopathy neurodegenerative diseases. MATERIALS AND METHODS: Using a systematic PubMed search, we identified 19 patients with lesions in different brain regions that caused RBD. First, lesion network mapping was applied to confirm whether the lesion locations causing RBD corresponded to a common brain network. Second, the literature-based RBD lesion network map was validated using neuroimaging findings and locations of brain pathologies at post-mortem in patients with idiopathic RBD (iRBD) who were identified by independent systematic literature search using PubMed. Finally, we assessed the locational relationship between the sites of pathological alterations at the preclinical stage in α-synucleinopathy neurodegenerative diseases and the brain network for RBD. RESULTS: The lesion network mapping showed lesions causing RBD to be localized to a common brain network defined by connectivity to the pons (including the locus coeruleus, dorsal raphe nucleus, central superior nucleus, and ventrolateral periaqueductal gray), regardless of the lesion location. The positive regions in the pons were replicated by the neuroimaging findings in an independent group of patients with iRBD and it coincided with the reported pathological alterations at post-mortem in patients with iRBD. Furthermore, all brain pathological sites at preclinical stages (Braak stages 1-2) in Parkinson's disease (PD) and at brainstem Lewy body disease in dementia with Lewy bodies (DLB) were involved in the brain network identified for RBD. CONCLUSION: The brain network defined by connectivity to positive pons regions might be the regulatory network loop inducing RBD in humans. In addition, our results suggested that the underlying cause of high phenoconversion rate from iRBD to neurodegenerative α-synucleinopathy might be pathological changes in the preclinical stage of α-synucleinopathy located at the regulatory network loop of RBD.

Lesions causing central sleep apnea localize to one common brain network.

Objectives: To characterize the specific brain regions for central sleep apnea (CSA) and identify its functional connectivity network. Methods: We performed a literature search and identified 27 brain injuries causing CSA. We used a recently validated methodology termed "lesion network mapping" to identify the functional brain network subtending the pathophysiology of CSA. Two separate statistical approaches, the two-sample t-test and the Liebermeister test, were used to evaluate the specificity of this network for CSA through a comparison of our results with those of two other neurological syndromes. An additional independent cohort of six CSA cases was used to assess reproducibility. Results: Our results showed that, despite lesions causing CSA being heterogeneous for brain localization, they share a common brain network defined by connectivity to the middle cingulate gyrus and bilateral cerebellar posterior lobes. This CSA-associated connectivity pattern was unique when compared with lesions causing the other two neurological syndromes. The CAS-specific regions were replicated by the additional independent cohort of six CSA cases. Finally, we found that all lesions causing CSA aligned well with the network defined by connectivity to the cingulate gyrus and bilateral cerebellar posterior lobes. Conclusion: Our results suggest that brain injuries responsible for CSA are part of a common brain network defined by connectivity to the middle cingulate gyrus and bilateral cerebellar posterior lobes, lending insight into the neuroanatomical substrate of CSA.

Fornix alterations induce the disruption of default mode network in patients with adamantinomatous craniopharyngiomas.

Adamantinomatous craniopharyngioma (ACPs) are rare embryonic tumors and often involve the hypothalamus. The underlying neural substrate of the hypothalamic involvement (HI)-related cognitive decline in patients with ACP is still unclear. We aimed to combine the multi-modal neuroimaging and histological characteristics of the ACP to explore the potential neural substrate of the HI-related cognitive decline. 45 patients with primary ACPs (invasive, 23; noninvasive, 22) and 52 healthy control subjects (HCs) were admitted to the cross-sectional study. No significant difference in cognitive domains was observed between HCs and patients with noninvasive ACPs (NACP). Patients with invasive ACPs (IACP) showed significantly lower working memory performance (WM, p = 0.002) than patients with NACP. The WM decline was correlated with the disruption of the medial temporal lobe (MTL) subsystem in the default mode network (DMN) (r = 0.45, p = 0.004). The increased radial diffusivity of the fornix, indicating demyelinating process, was correlated with the disruption of the MTL subsystem (r = -0.48, p = 0.002). Our study demonstrated that the fornix alterations link DMN disruption to HI-related cognitive decline in patients with ACPs. ACPs that invade the hypothalamus can provide a natural disease model to investigate the potential neural substrate of HI-related cognitive decline.

Arterial transit artifacts on arterial spin labeling MRI can predict cerebral hyperperfusion after carotid endarterectomy: an initial study.

OBJECTIVES: To investigate whether preoperative arterial spin labeling (ASL) MRI can predict cerebral hyperperfusion after carotid endarterectomy (CEA) in patients with carotid stenosis. METHODS: Consecutive patients with carotid stenosis who underwent CEA between May 2015 and July 2021 were included. For each patient, a cerebral blood flow ratio (rCBF) map was obtained by dividing postoperative CBF with preoperative CBF images from two pseudo-continuous ASL scans. Hyperperfusion regions with rCBF > 2 were extracted and weighted with rCBF to calculate the hyperperfusion index. According to the distribution of the hyperperfusion index, patients were divided into hyperperfusion and non-hyperperfusion groups. Preoperative ASL images were scored based on the presence of arterial transit artifacts (ATAs) in 10 regions of interest corresponding to the Alberta Stroke Programme Early Computed Tomography Score methodology. The degree of stenosis and primary and secondary collaterals were evaluated to correlate with the ASL score. Logistic regression and receiver operating characteristic curve analyses were performed to assess the predictive ability of the ASL score for cerebral hyperperfusion. RESULTS: Of 86 patients included, cerebral hyperperfusion was present in 17 (19.8%) patients. Carotid near occlusion, opening of posterior communicating arteries with incomplete anterior semicircle, and leptomeningeal collaterals were associated with lower ASL scores (p < 0.05). The preoperative ASL score was an independent predictor of cerebral hyperperfusion (OR = 0.48 [95% CI [0.33-0.71]], p < 0.001) with the optimal cutoff value of 25 points (AUC = 0.98, 94.1% sensitivity, 88.4% specificity). CONCLUSIONS: Based on the presence of ATAs, ASL can non-invasively predict cerebral hyperperfusion after CEA in patients with carotid stenosis. KEY POINTS: • Carotid near occlusion, opening of posterior communicating arteries with incomplete anterior semicircle, and leptomeningeal collaterals were associated with lower ASL scores. • The ASL score performed better than the degree of stenosis, type of CoW, and leptomeningeal collaterals, as well as the combination of the three factors for the prediction of cerebral hyperperfusion. • For patients with carotid stenosis, preoperative ASL can non-invasively identify patients at high risk of cerebral hyperperfusion after carotid endarterectomy without complex post-processing steps.

Ferroptosis in oligodendrocyte progenitor cells mediates white matter injury after hemorrhagic stroke.

Oligodendrocyte progenitor cells (OPCs) differentiate to myelin-producing mature oligodendrocytes and enwrap growing or demyelinated axons during development and post central nervous diseases. Failure of remyelination owing to cell death or undifferentiation of OPCs contributes to severe neurologic deficits and motor dysfunction. However, how to prevent the cell death of OPCs is still poorly understood, especially in hemorrhagic diseases. In the current study, we injected autologous blood into the mouse lateral ventricular to study the hemorrhage-induced OPC cell death in vivo. The integrity of the myelin sheath of the corpus callosum was disrupted post intraventricular hemorrhage (IVH) assessed by using magnetic resonance imaging, immunostaining, and transmission electron microscopy. Consistent with the severe demethylation, we observed massive cell death of oligodendrocyte lineages in the periventricular area. In addition, we found that ferroptosis is the major cell death form in Hemin-induced OPC death by using RNA-seq analysis, and the mechanism was glutathione peroxidase 4 activity reduction-resulted lipid peroxide accumulation. Furthermore, inhibition of ferroptosis rescued OPC cell death in vitro, and in vivo attenuated IVH-induced white matter injury and promoted recovery of neurological function. These data demonstrate that ferroptosis is an essential form of OPC cell death in hemorrhagic stroke, and rescuing ferroptotic OPCs could serve as a therapeutic target for stroke and related diseases.

A CNN-transformer hybrid approach for decoding visual neural activity into text.

BACKGROUND AND OBJECTIVE: Most studies used neural activities evoked by linguistic stimuli such as phrases or sentences to decode the language structure. However, compared to linguistic stimuli, it is more common for the human brain to perceive the outside world through non-linguistic stimuli such as natural images, so only relying on linguistic stimuli cannot fully understand the information perceived by the human brain. To address this, an end-to-end mapping model between visual neural activities evoked by non-linguistic stimuli and visual contents is demanded. METHODS: Inspired by the success of the Transformer network in neural machine translation and the convolutional neural network (CNN) in computer vision, here a CNN-Transformer hybrid language decoding model is constructed in an end-to-end fashion to decode functional magnetic resonance imaging (fMRI) signals evoked by natural images into descriptive texts about the visual stimuli. Specifically, this model first encodes a semantic sequence extracted by a two-layer 1D CNN from the multi-time visual neural activity into a multi-level abstract representation, then decodes this representation, step by step, into an English sentence. RESULTS: Experimental results show that the decoded texts are semantically consistent with the corresponding ground truth annotations. Additionally, by varying the encoding and decoding layers and modifying the original positional encoding of the Transformer, we found that a specific architecture of the Transformer is required in this work. CONCLUSIONS: The study results indicate that the proposed model can decode the visual neural activities evoked by natural images into descriptive text about the visual stimuli in the form of sentences. Hence, it may be considered as a potential computer-aided tool for neuroscientists to understand the neural mechanism of visual information processing in the human brain in the future.

The brain basis of handwriting deficits in Chinese children with developmental dyslexia.

Abundant behavioral studies have demonstrated high comorbidity of reading and handwriting difficulties in developmental dyslexia (DD), a neurological condition characterized by unexpectedly low reading ability despite adequate nonverbal intelligence and typical schooling. The neural correlates of handwriting deficits remain largely unknown; however, as well as the extent that handwriting deficits share common neural bases with reading deficits in DD. The present work used functional magnetic resonance imaging to examine brain activity during handwriting and reading tasks in Chinese dyslexic children (n = 18) and age-matched controls (n = 23). Compared to controls, dyslexic children exhibited reduced activation during handwriting tasks in brain regions supporting sensory-motor processing (including supplementary motor area and postcentral gyrus) and visual-orthography processing (including bilateral precuneus and right cuneus). Among these regions, the left supplementary motor area and the right precuneus also showed a trend of reduced activation during reading tasks in dyslexics. Moreover, increased activation was found in the left inferior frontal gyrus and anterior cingulate cortex in dyslexics, which may reflect more efforts of executive control to compensate for the impairments of motor and visual-orthographic processing. Finally, dyslexic children exhibited aberrant functional connectivity among brain areas for cognitive control and sensory-motor processes during handwriting tasks. Together, these findings suggest that handwriting deficits in DD are associated with functional abnormalities of multiple brain regions implicated in motor execution, visual-orthographic processing, and cognitive control, providing important implications for the diagnosis and treatment of dyslexia.

Altered cerebral perfusion and microstructure in advanced Parkinson's disease and their associations with clinical features.

OBJECTIVE: To explore the whole cerebral perfusion and microstructure alteration patterns in Parkinson's disease (PD) and the associations of these patterns with clinical features. METHODS: Forty-one subjects [20 PD patients and 21 healthy controls (HCs)] underwent arterial spin labeling (ASL), diffusion tensor imaging (DTI) and 3D T1-weighted imaging (T1WI) MRI. The cerebral blood flow (CBF) of the whole brain and the fractional anisotropy (FA), axial diffusivity (AD), radial diffusivity (RD) and mean diffusivity (MD) of subcortical and cerebellar regions were measured and compared between groups. Pearson's correlation was calculated between MRI measurements and clinical features [Unified Parkinson's Disease Rating Scale (UPDRS), UPDRS III, Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA) and olfactory test scores]. RESULTS: Compared to HCs, PD patients showed lower CBF in the frontal, parietal and temporal lobes but higher CBF in bilateral hippocampi, red nuclei, right substantia nigra, thalamus and most cerebellar regions. The MD in the right thalamus and several regions in the cerebellum increased in PD compared to HCs. In PD patients, the total UPDRS, UPDRS III, MoCA, MMSE and olfactory test scores were related to FA or CBF in cerebellum. (all p < 0.05). CONCLUSION: Hypoperfusion in cortical regions, together with hyperperfusion in subcortical and cerebellar regions may be the characteristic perfusion pattern in advanced PD patients. The microstructures of the right thalamus and cerebellum were changed in PD patients. The cognitive, motor and olfactory performance of PD patients is closely related to the perfusion and microstructure of the brain, especially the cerebellum.

Neural Mechanism Underlying the Sleep Deprivation-Induced Abnormal Bistable Perception.

Quality sleep is vital for physical and mental health. No matter whether sleep problems are a consequence of or contributory factor to mental disorders, people with psychosis often suffer from severe sleep disturbances. Previous research has shown that acute sleep deprivation (SD) can cause transient brain dysfunction and lead to various cognitive impairments in healthy individuals. However, the relationship between sleep disturbance and bistable perception remains unclear. Here, we investigated whether the bistable perception could be affected by SD and elucidated the functional brain changes accompanying SD effects on bistable perception using functional magnetic resonance imaging. We found that the 28-h SD resulted in slower perceptual transitions in healthy individuals. The reduced perceptual transition was accompanied by the decreased activations in rivalry-related frontoparietal areas, including the right superior parietal lobule, right frontal eye field, and right temporoparietal junction. We speculated that SD might disrupt the normal function of these regions crucial for bistable perception, which mediated the slower rivalry-related perceptual transitions in behavior. Our findings revealed the neural changes underlying the abnormal bistable perception following the SD. It also suggested that SD might offer a new window to understand the neural mechanisms underlying the bistable perception.

Aberrant Functional Connectivity of the Posterior Cingulate Cortex in Type 2 Diabetes Without Cognitive Impairment and Microvascular Complications.

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

Assessment of peripheral neuropathy in type 2 diabetes by diffusion tensor imaging: A case-control study.

OBJECTIVES: This study aimed to evaluate diabetes peripheral neuropathy (DPN) by diffusion tensor imaging (DTI) and explore the correlation between DTI parameters and electrophysiological parameters. METHODS: We examined tibial nerve (TN) and common peroneal nerve (CPN) of 32 DPN patients and 23 healthy controls using T1-weighted magnetic resonance imaging and DTI. Fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity (AD) and radial diffusivity (RD) of TN and CPN were measured and compared between groups. Spearman correlation coefficient was used to explore the relationship between DTI parameters and electrophysiology parameters in the DPN group. Diagnostic value was assessed by receiver operating characteristic (ROC) analysis. RESULTS: In the DPN group, FA was decreased (p < 0.0001) and MD and RD were increased (p < 0.05, p < 0.001) in the TN and CPN compared with the values of healthy control group. Moreover, in the DPN group, FA was positively correlated with motor nerve conduction velocity (MCV) (p < 0.0001), and both MD and RD were negatively correlated with MCV (p < 0.05, p < 0.001). However, there was no correlation between AD and any electrophysiological parameters. Among all DTI parameters, FA displayed the best diagnostic accuracy, with an area under the ROC curve of 0.882 in TN and 0.917 in CPN. CONCLUSION: FA and RD demonstrate appreciable diagnostic accuracy. Furthermore, they both have a moderate correlation with MCV.