Neurofunctional Changes Research Articles

Subjective cognitive decline is associated with altered patterns of brain activity and connectivity during performance of an old/new recognition memory task

IntroductionSubjective Cognitive Decline (SCD) is considered a preclinical stage within the AD continuum. Knowledge about the functional changes in the brain associated with episodic memory retrieval and novelty recognition in people with SCD is currently very limited. MethodThe study aimed to evaluate behavioural and neurofunctional changes in individuals with SCD, measured relative to a control group, during successful episodic memory retrieval and novelty recognition, as well as to compare the functional connectivity patterns related to these cognitive processes within the Default Mode Network (DMN) in both groups. Participants performed an old/new recognition memory task with words while the BOLD signal was acquired. ResultsNo between-group differences were observed in the performance of the episodic memory task. However, during the successful recognition of old words, the SCD group showed brain hypoactivity in the right rolandic operculum and reduced functional connectivity between the DMN and the fronto-parietal control network (FPCN). During the correct identification of new words, the SCD group also showed reduced connectivity between the DMN and the FPCN, and lower connectivity within the DMN. ConclusionDespite the absence of objective evidence of cognitive impairment, people with SCD display several changes in brain activity and connectivity associated with episodic memory retrieval and novelty recognition.

Resveratrol Protects Müller Cells Against Ferroptosis in the Early Stage of Diabetic Retinopathy by Regulating the Nrf2/GPx4/PTGS2 Pathway.

The aim of this study was to investigate the anti-ferroptotic effect of resveratrol (RSV) on retinal Müller cells (RMCs) in the early stages of diabetic retinopathy (DR) via the nuclear factor erythroid 2-related factor 2 (Nrf2)/glutathione peroxidase 4 (GPx4)/prostaglandin-endoperoxide synthase 2 (PTGS2). The retina was obtained from normal and diabetic Sprague-Dawley rats or wild-type and Nrf2 knockout (KO) diabetic mice, with or without RSV (10mg/kg/d) treatment for 12weeks. RMCs transfected with or without SiNrf2 were cultured with high glucose and RSV (20mM). The retinal neurofunctional changes were measured by electroretinogram (ERG). The retinal inner nuclear layer cell mitochondrial morphological changes were detected by transmission electron microscopy. The cell viabilities were measured by cell counting kit-8 (CCK-8) assay. The levels of Fe2+, malonic dialdehyde (MDA), and glutathione (GSH) were measured by colorimetric method. The expression of Nrf2, GPx4, and PTGS2 was detected by quantitative real-time polymerase chain reaction (qRT-PCR), western blotting, and immunocytochemistry. In vivo, RSV inhibited retinal neurofunctional changes and mitochondrial morphological changes; decreased Fe2+, MDA, and PTGS2; and increased GSH, Nrf2, and GPx4 in retina of DM rats. In vitro, RSV decreased MDA and PTGS2 and increased cell viability, GSH, Nrf2, and GPx4. In vivo and vitro, the role of Nrf2-regulated signaling pathway in anti-ferroptosis by RSV was further confirmed using Nrf2 KO mice and pre-transfected SiNrf2 in RMCs. These findings indicated that RSV is a potential therapeutic option for DR and that Nrf2/GPx4/PTGS2 plays a role in the anti-ferroptosis mechanism of RSV on RMCs.

Functional MRI Assessment of Brain Activity Patterns Associated with Reading in Medulloblastoma Survivors.

Medulloblastoma, a malignant brain tumor primarily affecting children, poses significant challenges to patients and clinicians due to its complex treatment and potential long-term cognitive consequences. While recent advancements in treatment have significantly improved survival rates, survivors often face cognitive impairments, particularly in reading, impacting their quality of life. According to the double deficit theory, reading impairments are caused by deficits in one or both of two independent reading-related functions: phonological awareness and rapid visual naming. This longitudinal study investigates neurofunctional changes related to reading in medulloblastoma survivors in comparison to controls using functional MRI acquired during rapid automatized naming tasks over three annual visits. Support vector machine classification of functional MRI data reveals a progressive divergence in brain activity patterns between medulloblastoma survivors and healthy controls over time, suggesting delayed effects of cancer treatment on brain function. Alterations in brain regions involved in visual processing and orthographic recognition during rapid naming tasks imply disruptions in the ventral visual pathway associated with normal orthographic processing. These alterations are correlated with performance in tasks involving sound awareness, reading fluency, and word attack. These findings underscore the dynamic nature of post-treatment neurofunctional alterations and the importance of early identification and intervention to address cognitive deficits in survivors.

Examining the Complex Mismatch Negativity in Early Phase Psychosis Using the Dual Rule Paradigm.

Using electroencephalography (EEG) to examine the simple mismatch negativity (MMN), a marker of auditory cortex function, has been of great interest in the exploration of biomarkers for psychotic illness. Despite many studies reporting MMN deficits in chronic schizophrenia, there are inconsistent reports of MMN reductions in the early phases of psychotic illness, suggesting the MMN elicited by traditional paradigms may not be a sensitive enough measure of vulnerability to be used as a biomarker. Recently, a more computationally complex measure of auditory cortex function (the complex mismatch negativity; cMMN) has been hypothesized to provide a more sensitive marker of illness vulnerability. The current study employed a novel dual rule paradigm, in which two pattern rules are established and violated, to examine the cMMN in 14 individuals with early phase psychosis (EPP, < 5 years illness) and 15 healthy controls (HC). Relationships between cMMN waveforms, symptom severity, and measures of functioning were explored. We found reductions of cMMN amplitudes at the site of maximal amplitude in EPP (p = .017) with large effect sizes (Hedges' g = 0.96). This study is an early step in the exploration of the cMMN as a biomarker for psychosis. Our results provide evidence that the dual rule cMMN paradigm shows promise as a method for cMMN elicitation that captures more subtle neurofunctional changes in the early stages of illness.

Prediction of adolescent idiopathic scoliosis with machine learning algorithms using brain volumetric measurements.

It is known that neuroanatomical and neurofunctional changes observed in the brain, brainstem and cerebellum play a role in the etiology of adolescent idiopathic scoliosis (AIS). This study aimed to investigate whether volumetric measurements of brain regions can be used as predictive indicators for AIS through machine learning techniques. Patients with a severe degree of curvature in AIS (n = 32) and healthy individuals (n = 31) were enrolled in the study. Volumetric data from 169 brain regions, acquired from magnetic resonance imaging (MRI) of these individuals, were utilized as predictive factors. A comprehensive analysis was conducted using the twelve most prevalent machine learning algorithms, encompassing thorough parameter adjustments and cross-validation processes. Furthermore, the findings related to variable significance are presented. Among all the algorithms evaluated, the random forest algorithm produced the most favorable results in terms of various classification metrics, including accuracy (0.9083), AUC (0.993), f1-score (0.970), and Brier score (0.1256). Additionally, the most critical variables were identified as the volumetric measurements of the right corticospinal tract, right corpus callosum body, right corpus callosum splenium, right cerebellum, and right pons, respectively. The outcomes of this study indicate that volumetric measurements of specific brain regions can serve as reliable indicators of AIS. In conclusion, the developed model and the significant variables discovered hold promise for predicting scoliosis development, particularly in high-risk individuals.

Neural Functioning in Late-Life Depression: An Activation Likelihood Estimation Meta-Analysis.

Late-life depression (LLD) is a relatively common and debilitating mental disorder, also associated with cognitive dysfunctions and an increased risk of mortality. Considering the growing elderly population worldwide, LLD is increasingly emerging as a significant public health issue, also due to the rise in direct and indirect costs borne by healthcare systems. Understanding the neuroanatomical and neurofunctional correlates of LLD is crucial for developing more targeted and effective interventions, both from a preventive and therapeutic standpoint. This ALE meta-analysis aims to evaluate the involvement of specific neurofunctional changes in the neurophysiopathology of LLD by analysing functional neuroimaging studies conducted on patients with LLD compared to healthy subjects (HCs). We included 19 studies conducted on 844 subjects, divided into 439 patients with LLD and 405 HCs. Patients with LLD, compared to HCs, showed significant hypoactivation of the right superior and medial frontal gyri (Brodmann areas (Bas) 8, 9), left cingulate cortex (BA 24), left putamen, and left caudate body. The same patients exhibited significant hyperactivation of the left superior temporal gyrus (BA 42), left inferior frontal gyrus (BA 45), right anterior cingulate cortex (BA 24), right cerebellar culmen, and left cerebellar declive. In summary, we found significant changes in activation patterns and brain functioning in areas encompassed in the cortico-limbic-striatal network in LLD. Furthermore, our results suggest a potential role for areas within the cortico-striatal-cerebellar network in the neurophysiopathology of LLD.

Longitudinal neurofunctional changes in medication overuse headache patients after mindfulness practice in a randomized controlled trial (the MIND-CM study)

BackgroundMindfulness practice has gained interest in the management of Chronic Migraine associated with Medication Overuse Headache (CM-MOH). Mindfulness is characterized by present-moment self-awareness and relies on attention control and emotion regulation, improving headache-related pain management. Mindfulness modulates the Default Mode Network (DMN), Salience Network (SN), and Fronto-Parietal Network (FPN) functional connectivity. However, the neural mechanisms underlying headache-related pain management with mindfulness are still unclear. In this study, we tested neurofunctional changes after mindfulness practice added to pharmacological treatment as usual in CM-MOH patients.MethodsThe present study is a longitudinal phase-III single-blind Randomized Controlled Trial (MIND-CM study; NCT03671681). Patients had a diagnosis of CM-MOH, no history of neurological and severe psychiatric comorbidities, and were attending our specialty headache centre. Patients were divided in Treatment as Usual (TaU) and mindfulness added to TaU (TaU + MIND) groups. Patients underwent a neuroimaging and clinical assessment before the treatment and after one year. Longitudinal comparisons of DMN, SN, and FPN connectivity were performed between groups and correlated with clinical changes. Vertex-wise analysis was performed to assess cortical thickness changes.Results177 CM-MOH patients were randomized to either TaU group or TaU + MIND group. Thirty-four patients, divided in 17 TaU and 17 TaU + MIND, completed the neuroimaging follow-up. At the follow-up, both groups showed an improvement in most clinical variables, whereas only TaU + MIND patients showed a significant headache frequency reduction (p = 0.028). After one year, TaU + MIND patients showed greater SN functional connectivity with the left posterior insula (p-FWE = 0.007) and sensorimotor cortex (p-FWE = 0.026). In TaU + MIND patients only, greater SN-insular connectivity was associated with improved depression scores (r = -0.51, p = 0.038). A longitudinal increase in cortical thickness was observed in the insular cluster in these patients (p = 0.015). Increased anterior cingulate cortex thickness was also reported in TaU + MIND group (p-FWE = 0.02).ConclusionsIncreased SN-insular connectivity might modulate chronic pain perception and the management of negative emotions. Enhanced SN-sensorimotor connectivity could reflect improved body-awareness of painful sensations. Expanded cingulate cortex thickness might sustain improved cognitive processing of nociceptive information. Our findings unveil the therapeutic potential of mindfulness and the underlying neural mechanisms in CM-MOH patients.Trial RegistrationName of Registry; MIND-CM study; Registration Number ClinicalTrials.gov identifier: NCT0367168; Registration Date: 14/09/2018

Neurofunctional changes related to methamphetamine and sexual cues in methamphetamine dependence from short- to long-term abstinence.

Abuse of methamphetamine has aroused concern worldwide. Stimulant use and sexual behaviours have been linked in behavioural and epidemiological studies. Although methamphetamine-related neurofunctional differences are reported in previous studies, only few studies have examined neurofunctional changes related to methamphetamine and sexual cues in methamphetamine dependence from short- to long-term abstinence. Neurofunctional changes were measured using a cue-reactivity task involving methamphetamine, sexual, and neutral cues in 20 methamphetamine abusers who were evaluated after a short- (1 week to 3 months) and long-term (10-15 months) abstinence. Five brain regions mainly involved in the occipital lobe and the parietal lobe were found with the group-by-condition interaction. Region-of-interest analyses found higher sexual-cue-related activation than other two activations in all five brain regions in the long-term methamphetamine abstinence group while no group differences were found. Negative relationships between motor impulsivity and methamphetamine- or sexual-cue-related activations in the left middle occipital gyrus, the superior parietal gyrus and the right angular gyrus were found. The findings suggested that methamphetamine abstinence may change the neural response of methamphetamine abusers to methamphetamine and sexual cues, and the neurofunction of the five brain regions reported in this study may partly recover with long-term methamphetamine abstinence. Given the use and relapse of methamphetamine for sexual purposes, the findings of this study may have particular clinical relevance.

Exploring the relationship between frailty and executive dysfunction: the role of frontal white matter hyperintensities.

Frailty is a geriatric syndrome frequently associated with executive dysfunction and white matter hyperintensities (WMH). But the relation between executive dysfunction and brain changes is poorly understood in frail subjects. Our hypothesis is that frontal-WMH mediates the association between frailty and executive dysfunction. A convenience sample of 113 subjects older than 65 years without dementia was studied with neuropsychological test, a structured clinical interview, physical examination and brain MRI. They were classified as robust or pre-frail and frail using the frailty phenotype score (0-5). The frontal WMH (F-WMH) were manually graduated (0-6) using the "Age-Related White Matter Changes score" from FLAIR sequences at a 3 Tesla brain MRI. A mediation analysis was done for testing whether F-WMH could act as a link factor between frailty phenotype score and executive dysfunction. The group's mean age was 74 ± 6 years, subjects with higher frailty score had more depressive symptoms and worse performance in executive function tests. A regression analysis that explained 52% of the variability in executive functions, revealed a significant direct effect of frailty score (Standardized βcoeff [95% CI] -0.201, [-0.319, -0.049], and F-WMH (-0.152[-0.269, -0.009]) on executive functions, while the F-WMH showed a small partial mediation effect between frailty and executive functions (-0.0395, [-0.09, -0.004]). Frontal matter hyperintensities had a small mediation effect on the association between frailty and executive dysfunction, suggesting that other neuropathological and neurofunctional changes might also be associated with executive dysfunction in frail subjects.

Brain amyloid-β deposition associated functional connectivity changes of ultra-large structural scale in mild cognitive impairment.

In preclinical Alzheimer's disease, neuro-functional changes due to amyloid-β (Aβ) deposition are not synchronized in different brain lobes and subcortical nuclei. This study aimed to explore the correlation between brain Aβ burden, connectivity changes in an ultra-large structural scale, and cognitive function in mild cognitive impairment. Participants with mild cognitive impairment were recruited and underwent florbetapir (F18-AV45) PET, resting-state functional MRI, and multidomain neuropsychological tests. AV-45 standardized uptake value ratio (SUVR) and functional connectivity of all participants were calculated. Of the total 144 participants, 72 were put in the low Aβ burden group and 72 in the high Aβ burden group. In the low Aβ burden group, all connectivities between lobes and nuclei had no correlation with SUVR. In the high Aβ burden group, SUVR showed negative correlations with the Subcortical-Occipital connectivity (r=-0.36, P = 0.02) and Subcortical-Parietal connectivity (r=-0.26, P = 0.026). Meanwhile, in the high Aβ burden group, SUVR showed positive correlations with the Temporal-Prefrontal connectivity (r = 0.27, P = 0.023), Temporal-Occipital connectivity (r = 0.24, P = 0.038), and Temporal-Parietal connectivity (r = 0.32, P = 0.006). Subcortical to Occipital and Parietal connectivities had positive correlations with general cognition, language, memory, and executive function. Temporal to Prefrontal, Occipital, and Parietal connectivities had negative correlations with memory function, executive function, and visuospatial function, and a positive correlation with language function. In conclusion, Individuals with mild cognitive impairment with high Aβ burden have Aβ-related bidirectional functional connectivity changes between lobes and subcortical nuclei that are associated with cognitive decline in multiple domains. These connectivity changes reflect neurological impairment and failed compensation.

Clinical case presentation on complex partial seizures diagnosis and treatment care services and outcomes in an adult patient

Complex partial seizure are often associated with impaired or loss of consciousness clinically proved to have an impact on masial temporal sclerosis (Hippocampus) region of brain. Seizures admits several etiopathophysiological events leading to several neuro functional changes in the reticulothalamocortical circuitry zones of the CNS .This paves the episodes of complex partial seizures events. A clinical case report of clinical partial seizures in a 47 years age adult patient came to the hospital with impaired consciousness. The brainmagnetic resonance imaging scanning of the patient detected a spectrum of findings more in favour of idiopathic intracranial hypertension and T1 ,T2 isointense lesion in the posterial mid line falx-2.falcine meningioma, focal area of glosis in the left high parietal lobe and age approximate bilateral cerebral atrophy it grade-1 fazellas white matter changes. The patient was conformed with Complex partial seizures, and she was treated with benzodiazepines twice a day. The patient was recovered from loss of impaired consciousness and she was called for follow up examination once in 1-month period.

Os exergames promovem alterações neurofuncionais na doença de Parkinson? Um estudo clínico piloto

Abstract Introduction Previous studies have demonstrated beneficial effects in people with Parkinson´s disease trained with exergames. However, to the best of our knowledge, none of them evaluated whether these effects are sustained by neurofunctional changes. Objective To evaluate neurofunctional effects of a training, by means of functional magnetic resonance imaging, in people with Parkinson´s disease. Methods This study was a blind, randomized, and controlled pilot clinical trial with crossover design. The participants were submitted to an evaluation including cognitive performance and functional magnetic resonance imaging before and after the WiiTM or control trainings. Trainings were applied for 10 days, in two consecutive weeks. Participants starting with WiiTM training were then moved to the control training and vice versa. A wash-out period of 45 days between the trainings was respected. Results Memory, executive and visuo-spatial functions, and attention were significantly improved compared to baseline (p &lt; 0.05). No differences were observed in cognition compared to the control training. Though not significant, results of functional magnetic resonance imaging analyses suggested that WiiTM training could promote improvements on the brain functional connectivity especially in areas involved in motor execution, planning, visual, memory and somatosensory functions. Conclusion In people with Parkinson´s disease, an intensive WiiTM training improved cognitive performance that underlined neurofunctional changes in areas involved in cognitive processing.

Towards a multidimensional model of inflamed depression

Major depressive disorder (MDD) continues to impose a significant burden on individuals and society. Existing data support the important role that inflammatory responses play in its pathophysiology, with new findings continuing to be reported. In this narrative review paper, we focus on three dimensions of inflamed depression: risk factors, clinical symptoms, and neurofunctional changes. We aim to answer the following questions: What characteristics most robustly discriminate between inflamed and non-inflamed depression? How can we leverage on these discriminative characteristics to classify inflamed depressed patients? One important point that has emerged is the heterogeneous nature of the relationship between inflammation and depression. Not all inflamed patients are depressed, and not all depressed patients are inflamed. Some risk factors heighten vulnerability to inflamed depression, including childhood adversity, old age, and being female. The inflamed depression subtype has been associated with distinct clinical phenotypes, most robustly with physical symptoms such as sleep problems, changes in appetite, and fatigue. Neurofunctional changes are found in the dopaminergic reward processing pathways. A better characterization of the inflamed depression subtype by leveraging multidimensional data will help craft a more precise treatment for these patients.

Investigation of Neurofunctional Changes Over the Course of Electroconvulsive Therapy.

Electroconvulsive therapy (ECT) is an effective treatment for patients suffering from depression. Yet the exact neurobiological mechanisms underlying the efficacy of ECT and indicators of who might respond best to it remain to be elucidated. Identifying neural markers that can inform about an individual's response to ECT would enable more optimal treatment strategies and increase clinical efficacy. Twenty-one acutely depressed inpatients completed an emotional working memory task during functional magnetic resonance imaging before and after receiving treatment with ECT. Neural activity was assessed in 5 key regions associated with the pathophysiology of depression: bilateral dorsolateral prefrontal cortex and pregenual, subgenual, and dorsal anterior cingulate cortex. Associations between brain activation and clinical improvement, as reflected by Montgomery-Åsberg Depression Rating Scale scores, were computed using linear regression models, t tests, and Pearson correlational analyses. Significant neurobiological prognostic markers or changes in neural activity from pre- to post ECT did not emerge. We could not confirm normalization effects and did not find significant neural markers related to treatment response. These results demonstrate that the search for reliable and clinically useful biomarkers for ECT treatment remains in its initial stages and still faces challenges.

Neurocircuitry of treatment in anxiety disorders.

Background:Understanding how treatments change neurobiology is critical to developing predictors of treatment response. This is especially true for anxiety disorders—the most common psychiatric disorders across the lifespan. With this in mind, we examined neurofunctional predictors of treatment response and neurofunctional changes associated with treatment across anxiety disorders.Methods:PubMed/Medline was searched for prospective treatment studies that included parallel examinations of functional activation or connectivity (both task-based and resting state) in adults and youth with panic disorder and generalized, separation, and/or social anxiety disorders published before April 30, 2021. All studies examining baseline predictors or changes related to pharmacologic and psychotherapeutic treatment of DSM-TV and DSM-5 anxiety disorders were included. Demographic, clinical, and treatment data as well as neurofunctional outcomes were extracted and summarized.Results:Twenty-nine studies examined changes in functional activation and/or connectivity (56 treatment arms) related to treatment and twenty-three examined neurofunctional predictors of treatment response. Predictors of treatment response and treatment-related neurofunctional changes were frequently observed within amygdala-prefrontal circuits. However, immense heterogeneity and few replication studies preclude a cohesive neurofunctional treatment response model across anxiety disorders.Conclusions:The extant literature describing neurofunctional aspects of treatment response in anxiety disorders is best viewed as a partially constructed scaffold on which to build a clinically translatable set of robust neuroimaging biomarkers that can be used to guide treatment and to select from available treatment. The construction of this understanding will require harmonization of analytic and task approaches, larger samples, and replication of component studies.

Study on the Association of Homocysteine and C-Reactive Protein with Neurofunctional Changes in Patients with Acute Ischemic Stroke After Endovascular Stent Treatment.

ObjectiveTo examine the association of homocysteine (HCY) and C-reactive protein (CRP) with neurofunctional changes in patients with acute ischemic stroke (AIS) after stent treatment.MethodsA total of 110 patients with AIS treated with stents were divided into a high HCY group (n = 59) and a normal HCY group (n = 51) based on the HCY level. Pearson correlation analysis and logistic linear regression analysis were used to analyze the related factors that affect the National Institutes of Health Stroke Scale (NIHSS) score changes after stent treatment.Results(1) The area under the receiver operating characteristic (ROC) curve for HCY was 0.995 (95% confidence interval [CI]: 0.984–1.005, P = 0.000), and the best predictive value was 12.75 µmol/L (sensitivity 89.9%, specificity 98.0%). The area under the ROC curve for CRP was 0.665 (95% CI: 0.564–0.767, P = 0.003), and the best predictive value was 9.7 mg/L; (2) comparison between the high HCY group and the normal HCY group showed statistical differences (P < 0.05) in HCY, CRP, and the NIHSS score at admission, the NIHSS score after treatment, gender, history of diabetes, and history of atrial fibrillation; (3) both HCY and CRP were proven to be correlated with the NIHSS score after treatment (0.188, P = 0.050) and (0.194, P = 0.042), respectively, using Pearson correlation analysis; (4) HCY, low-density lipoprotein, CRP, cystatin C, glucose, history of atrial fibrillation, history of diabetes, and the NIHSS score at admission as the risk factors.ConclusionHigh HCY and CRP levels are related to the neurofunctional changes in patients with AIS treated with stents and can be used as indicators to assess the risk of treating AIS with stents and as serum markers to predict prognoses.

EEG Power Band Asymmetries in Children with and without Classical Ensemble Music Training

Much evidence shows that music training influences the development of functional brain organization and cerebral asymmetry in an auditory-motor integrative neural system also associated with language and speech. Such overlap suggests that music training could be used for interventions in disadvantaged populations. Accordingly, we investigated neurofunctional changes associated with the influence of socially based classical ensemble music (CEM) training on executive auditory functions of children from low socioeconomic status (LSES), as compared to untrained counterparts. We conducted a novel ROI-focused reanalysis of stimulus-locked event-related electroencephalographic (EEG) band power data previously recorded from fifteen LSES children (9–10 years), with and without CEM, while performing a series of auditory Go/No-Go trials (involving 1100 Hz or 2000 Hz tones). An analysis of collapsed Alpha2, Beta1, Beta2, Delta, and Theta EEG bands showed significant differences in increased and decreased left asymmetry between the CEM and the Comparison group in key frontal and central electrodes typically associated with learning music. Overall, in Go trials, the CEM group responded more quickly and accurately. Linear regression analyses revealed both positive and negative correlations between left hemispheric asymmetry and behavioral measures of PPVT score, auditory sensitivity, Go accuracy, and reaction times. The pattern of results suggests that tone frequency and EEG asymmetries may be attributable to a shift to left lateralization as a byproduct of CEM. Our findings suggest that left hemispheric laterality associated with ensemble music training may improve the efficiency of productive language processing and, accordingly, may be considered as a supportive intervention for LSES children and youth.

Neural correlates of beneficial effects of young plasma treatment in aged mice: PET-SPM analyses and neuro-behavioural/molecular biological studies.

To investigate the in vivo neurofunctional changes and therapeutic effects of young blood plasma (YBP) in aged mice, as well as the molecular mechanisms underlying the therapeutic effects of YBP ex vivo and in vitro. Aged C57/BL6 mice received systemic administrations of phosphate-buffered saline (PBS) or YBP twice a week, for 4weeks. In vivo 2-[18F]-fluoro-2-deoxy-D-glucose positron emission tomography (18F-FDG PET) under conscious state and cognitive behavioural tests were performed after 4-week treatment. In addition, an in vitro senescent model was established, and the expressions of key cognition-associated proteins and/or the alterations of key neuronal pathways were analysed in both brain tissues and cultured cells. Aged mice treated with YBP demonstrated higher glucose metabolism in the right hippocampus and bilateral somatosensory cortices, and lower glucose metabolism in the right bed nucleus of stria terminalis and left cerebellum. YBP treatment exerted beneficial effects on the spatial and long-term social recognition memory, and significantly increased the expressions of several cognition-related proteins and altered the key neuronal signalling pathways in the hippocampus and somatosensory cortex. Further in vitro studies suggested that YBP but not aged blood plasma significantly upregulated the expressions of several cognition-associated proteins. Our results highlight the role of the hippocampus and somatosensory cortex in YBP-induced beneficial effects on recognition memory in aged mice. 18F-FDG PET imaging under conscious state provides a new avenue for exploring the mechanisms underlying YBP treatment against age-related cognitive decline.

Структурно-морфометрические и клинико-энцефалографические особенности эпилепсии у больных в позднем восстановительном периоде ишемического инсульта (обзор литературы)

Актуальность. В последние годы во всех странах отмечается существенный рост заболеваемости эпилепсией у лиц старших возрастных групп. Одним из наиболее частых факторов риска развития эпилептических припадков являются цереброваскулярные заболевания. Считается, что 10–30 % впервые диагностированных эпилептических припадков у пациентов старше 60 лет возникают после инсульта, что в дальнейшем значительно усложняет клиническую картину заболевания и служит причиной ухудшения качества жизни больных, замедляет восстановление потерянных вследствие инсульта функций, усиливает когнитивные и мнестические расстройства, увеличивает риск внезапной смерти, что, в свою очередь, требует пересмотра проводимой терапии с учетом фармакологического взаимодействия препаратов. Кроме того, достоверно установлено, что эпилептический приступ, который дебютировал в возрасте старше 60 лет, значительно увеличивает риск первичного и повторного инсульта. Несмотря на длительный период изучения данной проблемы, диагностика постинсультной эпилепсии (ПИЭ) затруднена до настоящего времени в связи с отсутствием единой позиции относительно понимания патогенеза, разной дефиницией диагноза, необъективной интерпретацией межприступной (интериктальной) электроэнцефалографии. Цель: провести анализ литературных данных относительно структурно-морфометрических и клинико-энцефалографических особенностей эпилепсии у больных в разные периоды ишемического инсульта. Проанализировать вероятность риска дебюта ПИЭ. Материалы и методы. Про-анализированы имеющиеся публикации, касающиеся вопросов ПИЭ, с помощью поиска, проведенного по таким базам данных, как Кокрановская база систематических обзоров (CDSR), центральный реестр контролируемых исследований Кокрана (CENTRAL), база данных SCOPUS и MEDLINE. Были отобраны соответствующие рандомизированные контролируемые исследования, однако из-за нехватки обзорных исследований и метаанализа в работу включены, в частности, наблюдательные и эпидемиологические исследования. Результаты. В большинстве проанализированных исследований авторы показали большую вариабельность частоты развития ПИЭ. Высокая вариабельность объясняется особенностями течения инсульта в разных популяциях, разной дефиницией диагноза ПИЭ, различным дизайном проведенных исследований. Однако в большинстве исследований было установлено, что риск развития ПИЭ удваивается от первого до пятого года после перенесенного инсульта и составляет около 4,2–5 %. Выводы. Таким образом, изучение нейрофункциональных и структурно-морфометрических изменений у больных эпилепсией в позднем восстановительном периоде ишемического инсульта является важной проблемой клинической неврологии, многие аспекты которой имеют в настоящее время неоднозначные, нередко противоречивые толкования. Поэтому изучение данной взаимосвязи позволит лучше понять патогенез ПИЭ, расширит возможности ее терапии и диагностики.

Dysregulated anterior insula reactivity as robust functional biomarker for chronic pain-Meta-analytic evidence from neuroimaging studies.

Neurobiological pain models propose that chronic pain is accompanied by neurofunctional changes that mediate pain processing dysfunctions. In contrast, meta‐analyses of neuroimaging studies in chronic pain conditions have not revealed convergent evidence for robust alterations during experimental pain induction. Against this background, the present neuroimaging meta‐analysis combined three different meta‐analytic approaches with stringent study selection criteria for case–control functional magnetic resonance imaging experiments during acute pain processing with a focus on chronic pain disorders. Convergent neurofunctional dysregulations in chronic pain patients were observed in the left anterior insula cortex. Seed‐based resting‐state functional connectivity based on a large publicly available dataset combined with a meta‐analytic task‐based approach identified the anterior insular region as a key node of an extended bilateral insula‐fronto‐cingular network, resembling the salience network. Moreover, the meta‐analytic decoding showed that this region presents a high probability to be specifically activated during pain‐related processes, although we cannot exclude an involvement in autonomic processes. Together, the present findings indicate that dysregulated left anterior insular activity represents a robust neurofunctional maladaptation and potential treatment target in chronic pain disorders.