Slowed information processing speed (IPS) is the core contributor to cognitive impairment in patients with late-life depression (LLD). The hippocampus is an important link between depression and dementia, and it may be involved in IPS slowing in LLD. However, the relationship between a slowed IPS and the dynamic activity and connectivity of hippocampal subregions in patients with LLD remains unclear.

One hundred thirty-four patients with LLD and 89 healthy controls were recruited. Sliding-window analysis was used to assess whole-brain dynamic functional connectivity (dFC), dynamic fractional amplitude of low-frequency fluctuations (dfALFF) and dynamic regional homogeneity (dReHo) for each hippocampal subregion seed.

Cognitive impairment (global cognition, verbal memory, language, visual–spatial skill, executive function and working memory) in patients with LLD was mediated by their slowed IPS. Compared with the controls, patients with LLD exhibited decreased dFC between various hippocampal subregions and the frontal cortex and decreased dReho in the left rostral hippocampus. Additionally, most of the dFCs were negatively associated with the severity of depressive symptoms and were positively associated with various domains of cognitive function. Moreover, the dFC between the left rostral hippocampus and middle frontal gyrus exhibited a partial mediation effect on the relationships between the scores of depressive symptoms and IPS.

Patients with LLD exhibited decreased dFC between the hippocampus and frontal cortex, and the decreased dFC between the left rostral hippocampus and right middle frontal gyrus was involved in the underlying neural substrate of the slowed IPS.

Wiedemann-Steiner syndrome (WSS) is a rare Mendelian disorder of the epigenetic machinery caused by heterozygous pathogenic variants in KMT2A. Currently, the specific neurocognitive profile of this syndrome remains unknown. This case series provides insight into the cognitive phenotype of WSS.

This study involves a retrospective medical chart review of 10 pediatric patients, each with a molecularly confirmed diagnosis of WSS who underwent clinical neuropsychological evaluation at an academic medical center.

The majority of patients performed in the below average to very low ranges in Nonverbal Reasoning, Visual/Spatial Perception, Visuoconstruction, Visual Memory, Attention, Working Memory and Math Computation skills. In contrast, over half the sample performed within normal limits on Receptive Vocabulary, Verbal Memory, and Word Reading. Wilcoxon signed rank test showed weaker Nonverbal versus Verbal Reasoning skills (p = .005). Most caregivers reported deficits in executive functioning, most notably in emotion regulation.

Nonverbal reasoning/memory, visuospatial/construction, attention, working memory, executive functioning, and math computation skills are areas of weakness among those with WSS. These findings overlap with research on Kabuki syndrome, which is caused by variants in KMT2D, and suggest disruption in the neurogenesis of the hippocampal formation may drive shared pathogenesis of the two syndromes.

No significant relationships.

The role of the white blood cells, which form the peripheral immune system and are crucial in inflammatory processes, has been laid aside in the context of brain structural changes in schizophrenia.

Determine how blood cells are associated with some brain structures volumes in first episode psychosis (FEP) and their relationship with clinical variables at baseline and 1 year follow – up.

Fifty drug-naïve FEP treated between April 2013 and July 2017 at the ETEP Program at Hospital del Mar were included. Inclusion criteria were: 1) age 18-35 years; 2) fulfillment of DSM-IV-TR criteria for brief psychotic disorder, schizophreniform disorder, schizophrenia or unspecified psychosis; 3) no previous history of severe neurological medical conditions or severe traumatic brain injury; 4) presumed IQ level > 80, and 5) no substance abuse or dependence disorders except for cannabis and/or nicotine use. All patients underwent an assessment at baseline and at one-year follow-up, including sociodemographic and clinical variables (substance use, DUP, PANSS, GAF and CDSS). Fasting blood samples were obtained before administering any medication at baseline. Structural T1 MRI was performed at baseline and brain volumes were quantified though FreeSurfer software. SPSS program was used for statistical analyzes.

Lymphocytes have a positive correlation with right and left hippocampus at baseline. Moreover, lymphocytes have a negative correlation with depressive symptoms at baseline and 1 year follow – up.

Lymphocytes may have a protective effect in some brain structures in FEP patients at baseline, especially those implicated in depressive symptoms.

No significant relationships.

The association between CYP2C19 poor metabolizer status, depressive symptom severity and hippocampal volume in humans is controversial. Progress in understanding not only the pathophysiology of depression but also potential protective mechanisms is important both for daily clinical practice and for the development of new antidepressant therapies.

To test and validate previous findings regarding the impact of CYP2C19 status on depressive symptoms and to examine whether it could influence hippocampus subregions and brain tissue microstructure.

A total of 4152 individuals from the Longitudinal cohort in the community-dwelling adult population - Colaus|PsyCoLaus in Lausanne, Switzerland were included. They have participated in at least one psychiatric evaluation. Brain anatomy patterns using a comprehensive set of psychometry, water diffusion- and relaxometry-based magnetic resonance imaging data were analysed in a subset of the cohort (BrainLaus, n=1187).

In this population-based cohort study, better lifetime global assessment of functioning scores were observed in poor metabolizers when compared to other metabolizers, this result was mainly driven by female participants (ß=3.9, P=0.01). Examination of brain imaging data revealed that higher right hippocampal subiculum volume was related to poor metabolizer status (ß=0.03, P=0.006). In addition, associations were observed between metabolizer status and white matter microstructure in the left uncinate fasciculus (ß=-0.01, P=0.01) and the left cingulum bundle (ß=-0.01, P=0.01).

CYP2C19 status is associated with modifications in lifetime global functioning, and brain anatomy. Such differences in brain structures can contribute to explain the protective effect of CYP2C19 poor metabolizer status.

No significant relationships.

The hippocampus is an important, complex limbic structure anatomically embedded in the medial temporal lobe of each cerebral cortex, which has been implicated in the pathogenesis of neuro-inflammatory disease conditions. Few studies have focused on the characterization of the MRI neuroimaging signatures of highly physio- pathologically relevant subfields of the hippocampus (CA1, CA4-DG, CA2/CA3, SLRM).

Using self-guided manually segmented, Diffusion weighted and NODDI maps created from data obtained from the Human Connectome Project (HCP) we intend to test whether Diffusion MRI-based quantitative imaging parameters (MD, FA, ODI, ISOVF, ICVF), indicative of microstructural characteristics of major hippocampal subfields (CA1, CA2/CA3, CA4-DG and SLRM), correspond to predictions for animal literature and imaging-histology correlations. We will also explore the correlations between these parameters and age.

We used images from the Public connectome data (updated April 2018), exploring subjects with the 3T MRI sessions obtainable from the WU-Minn HCP Data section. For the purpose of this study, we selected and downloaded 10 preliminary imaging data (6 females and 4 males) based on age variability in the following ranges (26-30, 31-35 and 36+). We manually segmented, and computed quantitative parameters.

Converging and consistent literature allude to decreasing volumes with increasing age. Analyzing the volumes from the diffusion maps (pilot data), this was also the case, with volumes computed from CA1 and DG-CA4 sub regions. IQT also allowed for better appreciation of neuroanatomical boundaries and land marks, hence allowing more regions to be easily manually segmented (addition of CA2/CA3).

Application to Neuroinflammatory imaging data.

No significant relationships.

Ample evidence suggests exercise is beneficial for hippocampal function. Furthermore, a single session of aerobic exercise provides immediate benefits to mnemonic discrimination performance, a highly hippocampal-specific memory process, in healthy younger adults. However, it is unknown if a single session of aerobic exercise alters mnemonic discrimination in older adults, who generally exhibit greater hippocampal deterioration and deficits in mnemonic discrimination performance.

We conducted a within subject acute exercise study in 30 cognitively healthy and physically active older adults who underwent baseline testing and then completed two experimental visits in which they performed a mnemonic discrimination task before and after either 30 min of cycling exercise or 30 min of seated rest. Linear mixed-effects analyses were conducted in which condition order and age were controlled, time (pre vs. post) and condition (exercise vs. rest) were modeled as fixed effects, and subject as a random effect.

No significant time by condition interaction effect was found for object recognition (p = .254, η2=.01), while a significant reduction in interference was found for mnemonic discrimination performance following the exercise condition (p = .012, η2=.07). A post-intervention only analysis indicated that there was no difference between condition for object recognition (p = .186, η2=.06), but that participants had better mnemonic discrimination performance (p < .001, η2=.22) following the exercise.

Our results suggest a single session of moderate-intensity aerobic exercise may reduce interference and elicit better mnemonic discrimination performance in healthy older adults, suggesting benefits for hippocampal-specific memory function.

The cognitive profile in 22q11.2 deletion syndrome (22q11.2DS) is often characterized by a discrepancy between nonverbal vs. verbal reasoning skills, in favor of the latter skills. This dissociation has also been observed in memory, with verbal learning skills described as a relative strength. Yet the development of these skills is still to be investigated. We thus aimed to explore verbal learning longitudinally. Furthermore, we explored verbal learning and its respective associations with hippocampal alterations and psychosis, which remain largely unknown despite their high prevalence in 22q11.2DS.

In total, 332 individuals (173 with 22q11.2DS) aged 5–30 years completed a verbal-paired associates task. Mixed-models regression analyses were conducted to explore developmental trajectories with threefold objectives. First, verbal learning and retention trajectories were compared between 22q11.2DS vs. HC. Second, we examined hippocampal volume development in 22q11.2DS participants with lower vs. higher verbal learning performance. Third, we explored verbal learning trajectories in 22q11.2DS participants with vs. without positive psychotic symptoms and with vs. without a psychotic spectrum disorder (PSD).

Our findings first reveal lower verbal learning performance in 22q11.2DS, with a developmental plateau emerging from adolescence. Second, participants with lower verbal learning scores displayed a reduced left hippocampal tail volume. Third, participants with PSD showed a deterioration of verbal learning performance, independently of verbal reasoning skills.

Our study challenges the current view of preserved verbal learning skills in 22q11.2DS and highlights associations with specific hippocampal alterations. We further identify verbal learning as a novel cognitive marker for psychosis in 22q11.2DS.

Anxiety can interfere with attention and working memory, which are components that affect learning. Statistical models have been designed to study learning, such as the Bayesian Learning Model, which takes into account prior possibilities and behaviors to determine how much of a new behavior is determined by learning instead of chance. However, the neurobiological basis underlying how anxiety interferes with learning is not yet known. Accordingly, we aimed to use neuroimaging techniques and apply a Bayesian Learning Model to study learning in individuals with generalized anxiety disorder (GAD).

Participants were 25 controls and 14 individuals with GAD and comorbid disorders. During fMRI, participants completed a shape-button association learning and reversal task. Using a flexible factorial analysis in SPM, activation in the dorsolateral prefrontal cortex, basal ganglia, and hippocampus were compared between groups during First Reversal. Beta values from the peak of these regions were extracted for all learning conditions and submitted to repeated measures analyses in SPSS.

Individuals with GAD showed less activation in the basal ganglia and the hippocampus only in the First Reversal compared with controls. This difference was not present in the Initial Learning and Second Reversal.

Given that the basal ganglia is associated with initial learning, and the hippocampus with transfer of knowledge from short to long term memory, our results suggest that GAD may engage these regions to a lesser extent during early accommodation or consolidation of learning, but have no longer term effects in brain activation patterns during subsequent learning.

Although many previous studies reported structural plasticity of the hippocampus and amygdala induced by electroconvulsive therapy (ECT) in major depressive disorder (MDD), yet the exact roles of both areas for antidepressant effects are still controversial.

In the current study, segmentation of amygdala and hippocampal sub-regions was used to investigate the longitudinal changes of volume, the relationship between volume and antidepressant effects, and prediction performances for ECT in MDD patients before and after ECT using two independent datasets.

As a result, MDD patients showed selectively and consistently increased volume in the left lateral nucleus, right accessory basal nucleus, bilateral basal nucleus, bilateral corticoamygdaloid transition (CAT), bilateral paralaminar nucleus of the amygdala, and bilateral hippocampus-amygdala transition area (HATA) after ECT in both datasets, whereas marginally significant increase of volume in bilateral granule cell molecular layer of the head of dentate gyrus, the bilateral head of cornu ammonis (CA) 4, and left head of CA 3. Correlation analyses revealed that increased volume of left HATA was significantly associated with antidepressant effects after ECT. Moreover, volumes of HATA in the MDD patients before ECT could be served as potential biomarkers to predict ECT remission with the highest accuracy of 86.95% and 82.92% in two datasets (The predictive models were trained on Dataset 2 and the sensitivity, specificity and accuracy of Dataset 2 were obtained from leave-one-out-cross-validation. Thus, they were not independent and very likely to be inflated).

These results not only suggested that ECT could selectively induce structural plasticity of the amygdala and hippocampal sub-regions associated with antidepressant effects of ECT in MDD patients, but also provided potential biomarkers (especially HATA) for effectively and timely interventions for ECT in clinical applications.

Animal studies have shown beneficial effects of probiotic supplementation on the hippocampus (HC) and cognitive performance. Evidence in humans is scarce. It was hypothesised that probiotic supplementation is associated with enhanced hippocampal (HC) regional grey matter volume (rGMV), as well as HC functional connectivity (FC). Relatedly improvements in mnestic and navigational performance, or emotional well-being, were expected to be observed in healthy human volunteers.

A randomised-controlled, double-blind trial (RCT) was conducted in N = 59 volunteers (age Mean = 27.1, s.d. = 6.7), applying a multi-strain probiotic (Vivomixx®) v. non-probiotic milk-powder placebo, each with 4.4 g/day, for 4 weeks. Volumetric data was extracted from 3T structural magnetic resonance images of total HC and -subfields. Voxel-based morphometry (VBM) and FreeSurfer-based analyses were performed. Potential neuroplastic change beyond HC was explored using whole-brain-VBM for white- and GMV. Seed-based FC was calculated based on HC. Cognitive tests included visual, map-based, object-location, and verbal memory, and spatial navigation. Mental health status (stress, anxiety, depression, and emotion-regulation) was assessed using self-reports.

There were no changes in HC-total, -subfield GMV, or FC, through probiotics. VBM revealed no changes at a whole-brain-level. There were no effects on cognitive performance or mental health. Evidence in favor of the null-hypothesis, using Bayesian statistics, was consistent.

The applied multi-strain probiotic did not elicit any effects concerning hippocampal structural plasticity, cognition, or mental well-being in young, healthy adults. For future studies, longer application/observation RCTs, perhaps in stressed, otherwise psychologically/ cognitively vulnerable, or ageing groups, with well-founded strain selection and investigation of mechanism, are advised.

Metabolic dysregulation is currently considered a major risk factor for hippocampal pathology. The aim of the present study was to characterize the influence of key metabolic drivers on functional connectivity of the hippocampus in healthy adults.

Insulin resistance was directly quantified by measuring steady-state plasma glucose (SSPG) concentration during the insulin suppression test and fasting levels of insulin, glucose, leptin, and cortisol, and measurements of body mass index and waist circumference were obtained in a sample of healthy cognitively intact adults (n = 104). Resting-state neuroimaging data were also acquired for the quantification of hippocampal functional cohesiveness and integration with the major resting-state networks (RSNs). Data-driven analysis using unsupervised machine learning (k-means clustering) was then employed to identify clusters of individuals based on their metabolic and functional connectivity profiles.

K-means clustering identified two clusters of increasing metabolic deviance evidenced by cluster differences in the plasma levels of leptin (40.36 (29.97) vs. 27.59 (25.58) μg/L) and the degree of insulin resistance (SSPG concentration: 161.63 (65.27) vs. 125.72 (66.81) mg/dL). Individuals in the cluster with higher metabolic deviance showed lower functional cohesiveness within each hippocampus and lower integration of posterior and anterior components of the left and right hippocampus with the major RSNs. The two clusters did not differ in general intellectual ability or episodic memory.

We identified two clusters of individuals differentiated by abnormalities in insulin resistance, leptin levels, and hippocampal connectivity, with one of the clusters showing greater deviance. These findings support the link between metabolic dysregulation and hippocampal function even in nonclinical samples.

Development of an acute cerebral dysfunction in a form of delirium after cardiac surgeries is common general medical problem that associated with prolonged hospital stay after the surgery, risk of development of infection, risk of subsequent neurocognitive changes, and postoperative morbidity

To compare risk of development of postoperative delirium in elderly patients with and without hippocampal dysfunction

Selective observational longitudinal study of the same group of objects in pre and postoperative period

For the diagnosis of degenerative process in CNS on early stages Free and cued selective reminding test immediate recall (FCSRT-IT) was shown to be the most sensitive. Based on learning of verbal material and semantic cues with recalling, FCSRT-IT allows differentiating amnestic disturbances hippocampal type from secondary disturbances of memory due to neurodynamic changes

Hippocampal dysfunction is a factor of developing of postoperative delirium in elderly patients that requires using additional measures in patients with mild cognitive disturbance to prevent developing of postoperative delirium

No significant relationships.