Amygdala In Patients Research Articles

Reduced gray matter volume of the hippocampal tail in melancholic depression: evidence from an MRI study

BackgroundMelancholic depression (MD) is one of the most prevalent and severe subtypes of major depressive disorder (MDD). Previous studies have revealed inconsistent results regarding alterations in grey matter volume (GMV) of the hippocampus and amygdala of MD patients, possibly due to overlooking the complexity of their internal structure. The hippocampus and amygdala consist of multiple and functionally distinct subregions, and these subregions may play different roles in MD. This study aims to investigate the volumetric alterations of each subregion of the hippocampus and amygdala in patients with MD and non-melancholic depression (NMD).MethodsA total of 146 drug-naïve, first-episode MDD patients (72 with MD and 74 with NMD) and 81 gender-, age-, and education-matched healthy controls (HCs) were included in the study. All participants underwent magnetic resonance imaging (MRI) scans. The subregional segmentation of hippocampus and amygdala was performed using the FreeSurfer 6.0 software. The multivariate analysis of covariance (MANCOVA) was used to detect GMV differences of the hippocampal and amygdala subregions between three groups. Partial correlation analysis was conducted to explore the relationship between hippocampus or amygdala subfields and clinical characteristics in the MD group. Age, gender, years of education and intracranial volume (ICV) were included as covariates in both MANCOVA and partial correlation analyses.ResultsPatients with MD exhibited a significantly lower GMV of the right hippocampal tail compared to HCs, which was uncorrelated with clinical characteristics of MD. No significant differences were observed among the three groups in overall and subregional GMV of amygdala.ConclusionsOur findings suggest that specific hippocampal subregions in MD patients are more susceptible to volumetric alterations than the entire hippocampus. The reduced right hippocampal tail may underlie the unique neuropathology of MD. Future longitudinal studies are required to better investigate the associations between reduced right hippocampal tail and the onset and progression of MD.

Hypoconnectivity of the Amygdala in Patients with Low-Back-Related Leg Pain Linked to Individual Mechanical Pain Sensitivity: A Resting-State Functional MRI Study.

To explore resting-state functional connectivity (rsFC) of the amygdala in patients with low-back-related leg pain (LBLP). For this prospective study, a total of 35 LBLP patients and 30 healthy controls (HCs) were included and underwent functional MRI and clinical assessments. Then, patients with LBLP were divided into acute LBLP (aLBLP) and chronic LBLP (cLBLP) subgroups. We further evaluated the between-group rsFC differences using left and right amygdala seeds in a whole-brain voxel analysis strategy. Finally, we performed correlation analysis between the rsFC values of altered regions and clinical indices. Compared to HCs, hypoconnectivity of the amygdala was observed in LBLP patients (P < 0.01, with correction). The amygdala's rsFC pattern was different between aLBLP and cLBLP patients: decreased the amygdala's FC to the right putamen, to the right paracentral lobule (PCL), or to the right posterior temporal lobe in aLBLP patients, while right amygdala to the bilateral anterior cingulate cortex (ACC) and the left postcentral gyrus (PoCG) in cLBLP patients. Correlation analysis showed that lower rsFC of the left amygdala to the right PCL was correlated with the von Frey filament (vF) test values of the left lumbar (p = 0.025) and right lumbar (p = 0.019) regions, and rsFC of the right amygdala to the left PoCG was correlated with lower vF test values of the left lumbar (p = 0.017), right lumbar spine (p = 0.003); to right PoCG was correlated with calf (p = 0.015); the rsFC of the right amygdala to bilateral ACC was negatively correlated with the pain rating index (p = 0.003). LBLP patients showed amygdala hypoconnectivity, and the altered pattern of amygdala rsFC was different in the acute and chronic phases. Moreover, the amygdala hypoconnectivity was related to individual mechanical sensitivity (vF test) in LBLP patients.

Hyperperfusion of bilateral amygdala in patients with chronic migraine: an arterial spin-labeled magnetic resonance imaging study

BackgroundAmygdala, an essential element of the limbic system, has served as an important structure in pain modulation. There is still a lack of clarity about altered cerebral perfusion of amygdala in migraine. This study aimed to investigate the perfusion variances of bilateral amygdala in episodic migraine (EM) and chronic migraine (CM) using multi-delay pseudo-continuous arterial spin-labeled magnetic resonance imaging (pCASL-MRI).MethodsTwenty-six patients with EM, 55 patients with CM (33 CM with medication overuse headache (MOH)), and 26 age- and sex-matched healthy controls (HCs) were included. All participants underwent 3D multi-delay pCASL MR imaging to obtain cerebral perfusion data, including arrival-time-corrected cerebral blood flow (CBF) and arterial cerebral blood volume (aCBV). The CBF and aCBV values in the bilateral amygdala were compared among the three groups. Correlation analyses between cerebral perfusion parameters and clinical variables were performed.ResultsCompared with HC participants, patients with CM were found to have increased CBF and aCBV values in the left amygdala, as well as increased CBF values in the right amygdala (all P < 0.05). There were no significant differences of CBF and aCBV values in the bilateral amygdala between the HC and EM groups, the EM and CM groups, as well as the CM without and with MOH groups (all P > 0.05). In patients with CM, the increased perfusion parameters of bilateral amygdala were positively correlated with MIDAS score after adjustments for age, sex, and body mass index (BMI).ConclusionHyperperfusion of bilateral amygdala might provide potential hemodynamics evidence in the neurolimbic pain network of CM.

Clinical Correlation of Altered Molecular Signatures in Epileptic Human Hippocampus and Amygdala

Widespread alterations in the expression of various genes could contribute to the pathogenesis of epilepsy. The expression levels of various genes, including major inhibitory and excitatory receptors, ion channels, cell type-specific markers, and excitatory amino acid transporters, were assessed and compared between the human epileptic hippocampus and amygdala, and findings from autopsy controls. Moreover, the potential correlation between molecular alterations in epileptic brain tissues and the clinical characteristics of patients undergoing epilepsy surgery was evaluated. Our findings revealed significant and complex changes in the expression of several key regulatory genes in both the hippocampus and amygdala of patients with intractable epilepsy. The expression changes in various genes differed considerably between the epileptic hippocampus and amygdala. Different correlation patterns were observed between changes in gene expression and clinical characteristics, depending on whether the patients were considered as a whole or were subdivided. Altered molecular signatures in different groups of epileptic patients, defined within a given category, could be viewed as diagnostic biomarkers. Distinct patterns of molecular changes that distinguish these groups from each other appear to be associated with epilepsy-specific functional consequences.

Volume alterations of the hippocampus and amygdala in patients with schizophrenia and persistent auditory hallucinations.

Auditory hallucinations (AH) are one of the most prevalent symptoms of schizophrenia. They might cause several brain alterations, especially changes in the volumes of hippocampus and amygdala, regions related to the relay and processing of auditory cues and emotional memories. We have recruited 41 patients with schizophrenia and persistent AH, 35 patients without AH, and 55 healthy controls. Using their MRIs, we have performed semiautomatic segmentations of the hippocampus and amygdala using Freesurfer. We have also performed bilateral correlations between the total PSYRATS score and the volumes of affected subregions and nuclei. In the hippocampus, we found bilateral increases in the volume of its hippocampal fissure and decreases in the right fimbria in patients with and without AH. The volume of the right hippocampal tail and left head of the granule cell layer from the dentate gyrus were decreased in patients with AH. In the amygdala, we found its left total volume was shrunk, and there was a decrease of its left accessory basal nucleus in patients with AH. We have detected volume alterations of different limbic structures likely due to the presence of AH. The volumes of the right hippocampal tail and left head of the granule cell layer from the dentate gyrus, and total volume of the amygdala and its accessory basal nucleus, were only affected in patients with AH. Bilateral volume alterations in the hippocampal fissure and right fimbria seem inherent of schizophrenia and due to traits not contemplated in our research.

Network analysis reveals abnormal functional brain circuitry in anxious dogs.

Anxiety is a common disease within human psychiatric disorders and has also been described as a frequently neuropsychiatric problem in dogs. Human neuroimaging studies showed abnormal functional brain networks might be involved in anxiety. In this study, we expected similar changes in network topology are also present in dogs. We performed resting-state functional MRI on 25 healthy dogs and 13 patients. The generic Canine Behavioral Assessment & Research Questionnaire was used to evaluate anxiety symptoms. We constructed functional brain networks and used graph theory to compare the differences between two groups. No significant differences in global network topology were found. However, focusing on the anxiety circuit, global efficiency and local efficiency were significantly higher, and characteristic path length was significantly lower in the amygdala in patients. We detected higher connectivity between amygdala-hippocampus, amygdala-mesencephalon, amygdala-thalamus, frontal lobe-hippocampus, frontal lobe-thalamus, and hippocampus-thalamus, all part of the anxiety circuit. Moreover, correlations between network metrics and anxiety symptoms were significant. Altered network measures in the amygdala were correlated with stranger-directed fear and excitability; altered degree in the hippocampus was related to attachment/attention seeking, trainability, and touch sensitivity; abnormal frontal lobe function was related to chasing and familiar dog aggression; attachment/attention seeking was correlated with functional connectivity between amygdala-hippocampus and amygdala-thalamus; familiar dog aggression was related to global network topology change. These findings may shed light on the aberrant topological organization of functional brain networks underlying anxiety in dogs.

Aberrant hippocampus and amygdala morphology associated with cognitive deficits in schizophrenia.

Working memory deficits are thought to be a primary disturbance in schizophrenia. We aimed to identify differences in morphology of the hippocampus and amygdala in patients with schizophrenia compared with healthy controls (HCs), and in patients who were either neuropsychologically near normal (NPNN) or neuropsychologically impaired (NPI). Morphological disturbances in the same subfields of the hippocampus and amygdala, but of greater magnitude in those with NPI, would strengthen evidence for the centrality of these limbic regions and working memory deficits in the pathogenesis of schizophrenia. We acquired anatomical MRIs in 69 patients with schizophrenia (18 NPNN, 46 NPI) and 63 age-matched HC participants. We compared groups in hippocampus and amygdala surface morphologies and correlated morphological measures with clinical symptoms and working memory scores. Schizophrenia was associated with inward deformations of the head and tail of the hippocampus, protrusion of the hippocampal body, and widespread inward deformations of the amygdala. In the same regions where we detected the effects of schizophrenia, morphological measures correlated positively with the severity of symptoms and inversely with working memory performance. Patients with NPI displayed a similar pattern of anatomical abnormality compared to patients with NPNN. Our findings indicate that anatomical abnormalities of the hippocampus relate to working memory performance and clinical symptoms in persons with schizophrenia. Moreover, NPNN and NPI patients may lie on a continuum of severity, both in terms of working memory abilities and altered brain structure, with NPI patients being more severe than NPNN patients in both domains.

Is abnormal metabolism in the olfactory bulb and amygdala associated with bipolar disorder?

Accumulated evidence has demonstrated abnormal amygdala activation in bipolar disorder (BD). The olfactory bulb (OB) has vigorous connections with the amygdala. Although odor-related functions of the OB decreased during the evolutionary process, we hypothesized that an evolved OB with increased activation in emotion regulation may be one of the main factors affecting amygdala functions in BD. Our aim was to investigate metabolism in the OB and amygdala in patients with BD. Twenty-six patients diagnosed with BD according to DSM-5 diagnostic criteria were included in this cross-sectional study. Metabolism in the OB and amygdala was assessed using fluorodeoxyglucose positron emission tomography/CT in patients with BD. The OB and amygdala metabolism was compared with the patients' Z scores. Both OB and amygdala metabolic activities were significantly higher than in the controls. A positive correlation was detected between right/left amygdala metabolism and right OB metabolism (p < 0.05, r:467 and r:662, respectively). This study increased our understanding of the etiopathogenesis of BD. In BD, the main cause of hypermetabolism in the amygdala may be increased metabolism in the OB. During evolution, the OB may have assumed a dominant role in emotional processing rather than olfactory functions.

Occupational stress is associated with sex and subregion specific modifications of the amygdala volumes

Background: Despite the rapid increase in reports of exhaustion syndrome (ES) due to daily occupational stress, the mechanisms underlying ES are unknown. In the present study, we investigated whether occupational ES is associated with specific modifications of the subfields of the amygdala and hippocampus resembling those described in other chronic stress conditions. Special focus was paid to possible sex differences. Methods: As a follow up to our previous studies of occupational ES, we carried out MRI-based subfield segmentation of the hippocampus and amygdala volumes in 58 patients with occupational ES (22 males) and 65 age-matched controls (27 males) (age range 30–46 years). Results: There was a significant and bilateral enlargement of the lateral, basal and central nucleus of the amygdala in patients with ES (corrected for the total intracranial volume (ICV)). These differences were detected only in females. Higher values in the right central and right basal amygdala remained when the whole amygdala volume was used as reference, instead of the ICV. Notably, in female patients the volumes of these specific nuclei were positively correlated with the degree of perceived stress. No changes in the hippocampus subfields were detected in female or male patients. Conclusions: The findings underline that ES is a chronic stress condition, suggesting that not only extreme forms of stress, but also the everyday stress is associated with localized differences from controls in the amygdala. The absence of significant alterations among men with ES despite a similar degree of perceived stress supports the notion that women seem more susceptible to stress-related cerebral changes, and may explain the higher prevalence of ES among women.

Abnormal amygdala functional connectivity and deep learning classification in multifrequency bands in autism spectrum disorder: A multisite functional magnetic resonance imaging study.

Previous studies have explored resting-state functional connectivity (rs-FC) of the amygdala in patients with autism spectrum disorder (ASD). However, it remains unclear whether there are frequency-specific FC alterations of the amygdala in ASD and whether FC in specific frequency bands can be used to distinguish patients with ASD from typical controls (TCs). Data from 306 patients with ASD and 314 age-matched and sex-matched TCs were collected from 28 sites in the Autism Brain Imaging Data Exchange database. The bilateral amygdala, defined as the seed regions, was used to perform seed-based FC analyses in the conventional, slow-5, and slow-4 frequency bands at each site. Image-based meta-analyses were used to obtain consistent brain regions across 28 sites in the three frequency bands. By combining generative adversarial networks and deep neural networks, a deep learning approach was applied to distinguish patients with ASD from TCs. The meta-analysis results showed frequency band specificity of FC in ASD, which was reflected in the slow-5 frequency band instead of the conventional and slow-4 frequency bands. The deep learning results showed that, compared with the conventional and slow-4 frequency bands, the slow-5 frequency band exhibited a higher accuracy of 74.73%, precision of 74.58%, recall of 75.05%, and area under the curve of 0.811 to distinguish patients with ASD from TCs. These findings may help us to understand the pathological mechanisms of ASD and provide preliminary guidance for the clinical diagnosis of ASD.

The hypertrophic amygdala shape associated with anxiety in patients with primary dysmenorrhea during pain-free phase: insight from surface-based shape analysis

BackgroundPrimary dysmenorrhea (PDM) is highly associated with mood symptoms. However, the neuropathology of these comorbidities is unclear. In the present study, we aimed to investigate the structural changes in the amygdala of patients with PDM during the pain-free phase using a surface-based shape analysis.MethodsForty-three PDM patients and forty healthy controls were recruited in the study, and all participants underwent structural magnetic resonance imaging scans during their periovulatory phase. FMRIB’s Integrated Registration and Segmentation Tool (FIRST) was employed to assess the subcortical volumetric and surface alterations in patients with PDM. Moreover, correlation and mediation analyses were used to detect the clinical significance of the subcortical morphometry alteration.ResultsPDM patients showed hypertrophic alteration of the amygdala in the left superficial nuclei and right basolateral and superficial nuclei but not for the whole amygdala volume. The hypertrophic amygdala was associated with disease duration, pain severity and anxiety symptoms during the menstrual period. Furthermore, the hypertrophic left amygdala could mediate the association between disease duration and anxiety severity.ConclusionsThe results of the current study demonstrated that the localized amygdala shape hypertrophy was present in PDM patients even in the pain-free phase. In addition, the mediator role of the hypertrophic amygdala indicates the potential target of amygdala for anxiety treatment in PDM treatment in the pain-free phase.

Characterization of a Novel Monoclonal Antibody for Serine-129 Phosphorylated α-Synuclein: A Potential Application for Clinical and Basic Research.

The Lewy bodies (LBs) are the pathological hallmark of Parkinson's disease (PD). More than 90% of α-synuclein (α-syn) within LBs is phosphorylated at the serine-129 residue [pSer129 α-syn (p-α-syn)]. Although various studies have revealed that this abnormally elevated p-α-syn acts as a pathological biomarker and is involved in the pathogenic process of PD, the exact pathophysiological mechanisms of p-α-syn are still not fully understood. Therefore, the development of specific and reliable tools for p-α-syn detection is important. In this study, we generated a novel p-α-syn mouse monoclonal antibody (C140S) using hybridoma technology. To further identify the characteristics of C140S, we performed several in vitro assays using recombinant proteins, along with ex vivo assays utilizing the brains of Thy1-SNCA transgenic (Tg) mice, the preformed fibril (PFF)-treated neurons, and the brain sections of patients with PD. Our C140S specifically recognized human and mouse p-α-syn proteins both in vitro and ex vivo, and similar to commercial p-α-syn antibodies, the C140S detected higher levels of p-α-syn in the midbrain of the Tg mice. Using immunogold electron microscopy, these p-α-syn particles were partly deposited in the cytoplasm and colocalized with the outer mitochondrial membrane. In addition, the C140S recognized p-α-syn pathologies in the PFF-treated neurons and the amygdala of patients with PD. Overall, the C140S antibody was a specific and potential research tool in the detection and mechanistic studies of pathogenic p-α-syn in PD and related synucleinopathies.

Smaller volume and altered functional connectivity of the amygdala in patients with lifelong premature ejaculation.

To analyze the abnormal amygdala structure and function in lifelong premature ejaculation (PE) patients compared with healthy controls (HCs). Forty-four lifelong PE patients and thirty-one HCs were enrolled in this study. Each subject was diagnosed with PE using a Premature Ejaculation Diagnostic Tool (PEDT) and intravaginal ejaculation latency time (IELT) score. Based on t-tests and Pearson correlation analysis, the voxel-based morphometry and functional connectivity (FC) analyses were applied to evaluate brain structural and functional changes by using T1-weighted and resting-state functional magnetic resonance imaging scans. Lifelong PE patients had decreased gray matter volume in the bilateral amygdala and increased FC between the amygdala and precuneus, posterior cingulate cortex (PCC), and middle temporal cortex (MTC), as well as decreased FC between the amygdala and precentral gyrus, insula, and inferior frontal gyrus. Moreover, significantly negative correlations between the IELT score and the mean z-score from amygdala-MTC (r = -0.49) and amygdala-PCC (r = -0.48) FC were found in lifelong PE patients. Our study investigated the abnormal amygdala-related structure and connectivity patterns in PE patients, which might provide novel perspective for understanding the crucial role of the amygdala in the neural mechanism of PE. • As one of the most common diseases in men, PE may be related to abnormal brain mechanisms. • Functional and structural magnetic resonance imaging used to explore amygdala abnormalities in PE patients. • The correlation between clinical scores and functional connectivity was used to assess the reasonability of the results.

Atrophy in the Left Amygdala Predicted Drug Responses in Idiopathic Generalized Epilepsy Patients With Tonic-Clonic Seizures.

We aimed to determine the alterations in the subcortical structures of patients with idiopathic generalized epilepsy with tonic–clonic seizures (IGE-GTCS) via MRI volumetry and vertex-based shape analysis and to evaluate the relationships between MRI measures and drug responses. In a follow-up sample of 48 patients with IGE-GTCS and 48 matched normal controls (NCs), high-resolution 3D T1WI was performed at baseline. After 1 year of follow-up, 31 patients were classified as seizure free (SF) and 17 as drug resistant (DR). The volumes of subcortical structures were extracted, and vertex-based shape analysis was performed using FSL-Integrated Registration and Segmentation Toolbox (FSL-FIRST). Comparisons among groups were calculated adjusting for covariates [age, sex, and intracranial volume (ICV)]. Analysis of the relationships among imaging biomarkers along with frequency and duration was assessed using partial correlations. The differential imaging indicators were used as features in a linear support vector machine (LSVM). The DR group displayed significant regional atrophy in the volume of the left amygdala compared with NCs (p = 0.004, false discovery rate corrected) and SF patients (p = 0.029, uncorrected). Meanwhile, vertex-based shape analysis showed focal inward deformation in the basolateral subregion of the left amygdala in DR compared with the results for SF and NC (p < 0.05, FWE corrected). There were significant correlations between the volume changes and seizure frequency (r = −0.324, p = 0.030) and between shape (r = −0.438, p = 0.003) changes and seizure frequency. Moreover, the volume of the left thalamus in the DR group was significantly correlated with seizure frequency (r = −0.689, p = 0.006). The SVM results revealed areas under the receiver operating characteristic curve of 0.82, 0.68, and 0.88 for the classification between SF and DR, between SF and NC, and between DR and NC, respectively. This study indicates the presence of focal atrophy in the basolateral region of the left amygdala in patients with IGE drug resistance; this finding may help predict drug responses and suggests a potential therapeutic target.

Seizure-related apneas have an inconsistent linkage to amygdala seizure spread.

Sudden unexpected death in epilepsy (SUDEP) is a frequent cause of death in epilepsy. Respiratory dysfunction is implicated as a critical factor in SUDEP pathophysiology. Human studies have shown that electrical stimulation of the amygdala resulted in apnea, indicating that the amygdala has a role in respiration control. Unilateral amygdala stimulation resulted in immediate onset of respiratory dysfunction occurring only during nose breathing. In small numbers of patients, some but not all spontaneous seizures resulted in apnea occurring shortly after seizure spread to the amygdala. With this study we aimed to determine whether seizure onset or spread to the amygdala was necessary and sufficient to cause apnea. We investigated the temporal relationship between apnea/hypopnea (AH) onset and initial seizure involvement within the amygdala in patients with implanted depth electrodes. Data from 17 patients (11 female) with 47 seizures were analyzed. With seven seizures (three patients), AH preceded amygdala seizure involvement by 2 to 55seconds. There was no AH with four seizures (three patients) that involved the amygdala. With eight seizures (four patients) AH occurred within 2seconds following amygdala seizure onset. With 28 seizures, AH started >2seconds after amygdala seizure onset (range 3-158seconds). Following seizure onset, there was a significant difference between AH onset time and amygdala seizure onset (P<.001). The mean ± standard deviation (SD) AH onset was 27.8±41.06seconds, and the mean time to amygdala involvement was 8.83±20.19seconds. There is a wide range of AH onset times relative to amygdala seizure involvement. With some seizures, amygdala seizure involvement occurs without AH. With other seizures, AH precedes amygdala seizures, suggesting that, with spontaneous seizures, involvement of the amygdala may not be crucial to induction of AH with all seizures. Other pathophysiology impacting brainstem respiratory networks may be of greater relevance to seizure-triggered apneas.

The relation between neuronal firing, local field potentials and hemodynamic activity in the human amygdala in response to aversive dynamic visual stimuli

The amygdala is a central part of networks of brain regions underlying perception and cognition, in particular related to processing of emotionally salient stimuli. Invasive electrophysiological and hemodynamic measurements are commonly used to evaluate functions of the human amygdala, but a comprehensive understanding of their relation is still lacking. Here, we aimed at investigating the link between fast and slow frequency amygdalar oscillations, neuronal firing and hemodynamic responses. To this aim, we recorded intracranial electroencephalography (iEEG), hemodynamic responses and single neuron activity from the amygdala of patients with epilepsy. Patients were presented with dynamic visual sequences of fearful faces (aversive condition), interleaved with sequences of neutral landscapes (neutral condition). Comparing responses to aversive versus neutral stimuli across participants, we observed enhanced high gamma power (HGP, >60 ​Hz) during the first 2 ​s of aversive sequence viewing, and reduced delta power (1–4 ​Hz) lasting up to 18 ​s. In 5 participants with implanted microwires, neuronal firing rates were enhanced following aversive stimuli, and exhibited positive correlation with HGP and hemodynamic responses. Our results show that high gamma power, neuronal firing and BOLD responses from the human amygdala are co-modulated. Our findings provide, for the first time, a comprehensive investigation of amygdalar responses to aversive stimuli, ranging from single-neuron spikes to local field potentials and hemodynamic responses.

Modulation of NMDA receptor by miR-219 in the amygdala and hippocampus of patients with mesial temporal lobe epilepsy

Mesial temporal lobe epilepsy with hippocampal sclerosis is the most frequent form of focal epilepsy in adults, and it is often refractory to drug treatment. Regardless of the efforts on developing new antiepileptic drugs for refractory cases, studies suggest a need for better understanding the molecular bases of epilepsy. The microRNAs have been progressively investigated as potential targets for both epilepsy mechanisms elucidation and treatment. Therefore, the goal of this study was to evaluate the differential expression of miR-219, miR-181b, and miR-195, previously described as regulators of the excitatory neurotransmitter receptors NMDA-R1 and AMPA-GluR2 and inhibitory neurotransmitter GABAA (α2, β3, and γ2 subunits) in the amygdala and hippocampus of patients with mesial temporal lobe epilepsy. Based on genes and miRNAs’ quantitative Polymerase Chain Reaction (qPCR) from 18 patients with epilepsy, our results showed an inverse relationship between miR-219 and NMDA-NR1 expression in both the amygdala and hippocampus in comparison to their expression in controls. NR1 and GluR2 were upregulated in the amygdala of epileptic patients. Low miR-195 expression was observed in the amygdala of patients with epilepsy. Our findings indicate that miR-219 has a possible regulatory role in excitatory neurotransmission in patients with epilepsy, contributing to the new avenue of miRNA biology in drug-resistant epilepsy, reserving huge potential for future applications and clinical interventions in conjunction with existing therapies.

Trust and the city: Linking urban upbringing to neural mechanisms of trust in psychosis.

Elevated prevalence of non-affective psychotic disorders is often found in densely populated areas. This functional magnetic resonance imaging study investigates if reduced trust, a component of impaired social functioning in patients with psychotic disorder, is associated with urban upbringing. In total, 39 patients (22 first episode and 17 clinical high risk) and 30 healthy controls, aged 16-29, performed two multi-round trust games, with a cooperative and unfair partner during functional magnetic resonance imaging scanning. Baseline trust was operationalized as the first investment made, and changes of trust as changes in investments made over the 20 trials during the games. Urban exposure during upbringing (0-15 years) was defined as higher urban (≥2500 inhabitants/km2) or lower urban (<2500 inhabitants/km2). Patients displayed lower baseline trust (first investment) than controls, regardless of urbanicity exposure. During cooperative interactions, lower-urban patients showed increasing investments. In addition, during cooperative interactions, group-by-developmental urbanicity interactions were found in the right and left amygdalae, although for the latter only at trend level. Higher urbanicity was associated with decreased activation of the left amygdala in patients and controls during investments and with increased activation of the right and left amygdalae in patients only, during repayments. During unfair interactions, no associations of urbanicity with behavior or brain activation were found. Urban upbringing was unrelated to baseline trust. Associations with urbanicity were stronger for patients compared to controls, suggesting greater susceptibility to urbanicity effects during the developmental period. Higher-urban patients failed to compensate for the initial distrust specifically during repeated cooperative interactions. This finding highlights potential implications for social functioning. Urban upbringing was linked to differential amygdala activation, suggesting altered mechanisms of feedback learning, but this was not associated with trust game behavior.

Study on the sub-regions volume of hippocampus and amygdala in schizophrenia.

Many studies have found volume changes in the hippocampus and amygdala in patients with schizophrenia, but these findings have not reached an agreement. Particularly, few results showed the volumes of the sub-regions of the amygdala. In this research, we aim to clarify volume changes of hippocampus and amygdala sub-regions in patients with schizophrenia. The sample consisted of 69 patients with schizophrenia and 72 control subjects aged from 18 to 65 years. FreeSurfer 6.0 software was used on T1-weighted images to assess the volumes of hippocampus and amygdala and their sub-regions. The general linear model (GLM) was used to analyze the volume changes between the two groups. False discovery rate (FDR) correction was performed, and the significance level was set at 0.05. The hippocampus volume in schizophrenia showed reduction compared to healthy control (P<0.05). Several hippocampal subfields showed smaller volume in schizophrenia patients, including bilateral presubiculum and molecular layer, left hippocampal tail, subiculum and cornus ammonis (CA)1, and right parasubiculum (P<0.05). Left amygdala volume showed a decrease as well, sub-regions including the bilateral basal nucleus, anterior-amygdaloid-area (AAA), paralaminar nucleus and left lateral nucleus (P<0.05). Several sub-regions of hippocampus and amygdala showed a volumetric decline in patients group, which suggest the key roles of these regions in the pathophysiology of schizophrenia. Based on these results, we speculate that these regions could be used to assess the early finding of schizophrenia.

Hippocampus and amygdalar volumes in patients with obsessive-compulsive personality disorder

ObjectivesMoving from the point that there might be an association between the neuroanatomy of obsessive-compulsive disorder (OCD) and obsessive-compulsive personality disorder, we decided to examine the volumes of hippocampus and amygdala of patients with obsessive-compulsive personality disorder, which was previously evaluated in OCD patients by us. MethodsVolumes of the hippocampus, and amygdala were measured by magnetic resonance imaging (MRI) in patients with obsessive-compulsive personality disorder and healthy control subjects. Manual tracing was used. ResultsWe detected that the mean left and right sides of hippocampus and amygdala volumes of the patients with obsessive-compulsive personality disorder were smaller than those of the healthy controls. ConclusionConsequently, our present results suggest that hippocampal and amygdalar structural abnormalities may be related to the neuroanatomy of obsessive-compulsive personality disorder. However, it is required novel studies with larger sample.