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Frontiers in Aging Neuroscience 2023Mild cognitive impairment (MCI) depicts a transitory phase between healthy elderly and the onset of Alzheimer's disease (AD) with worsening cognitive impairment. Some...
BACKGROUND
Mild cognitive impairment (MCI) depicts a transitory phase between healthy elderly and the onset of Alzheimer's disease (AD) with worsening cognitive impairment. Some functional MRI (fMRI) research indicated that the frontoparietal network (FPN) could be an essential part of the pathophysiological mechanism of MCI. However, damaged FPN regions were not consistently reported, especially their interactions with other brain networks. We assessed the fMRI-specific anomalies of the FPN in MCI by analyzing brain regions with functional alterations.
METHODS
PubMed, Embase, and Web of Science were searched to screen neuroimaging studies exploring brain function alterations in the FPN in MCI using fMRI-related indexes, including the amplitude of low-frequency fluctuation, regional homogeneity, and functional connectivity. We integrated distinctive coordinates by activating likelihood estimation, visualizing abnormal functional regions, and concluding functional alterations of the FPN.
RESULTS
We selected 29 studies and found specific changes in some brain regions of the FPN. These included the bilateral dorsolateral prefrontal cortex, insula, precuneus cortex, anterior cingulate cortex, inferior parietal lobule, middle temporal gyrus, superior frontal gyrus, and parahippocampal gyrus. Any abnormal alterations in these regions depicted interactions between the FPN and other networks.
CONCLUSION
The study demonstrates specific fMRI neuroimaging alterations in brain regions of the FPN in MCI patients. This could provide a new perspective on identifying early-stage patients with targeted treatment programs.
SYSTEMATIC REVIEW REGISTRATION
https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42023432042, identifier: CRD42023432042.
PubMed: 37448688
DOI: 10.3389/fnagi.2023.1165908 -
The conscious processing of emotion in depression disorder: a meta-analysis of neuroimaging studies.Frontiers in Psychiatry 2023Depression is generally accompanied by a disturbed conscious processing of emotion, which manifests as a negative bias to facial/voice emotion information and a...
BACKGROUND
Depression is generally accompanied by a disturbed conscious processing of emotion, which manifests as a negative bias to facial/voice emotion information and a decreased accuracy in emotion recognition tasks. Several studies have proved that abnormal brain activation was responsible for the deficit function of conscious emotion recognition in depression. However, the altered brain activation related to the conscious processing of emotion in depression was incongruent among studies. Therefore, we conducted an activation likelihood estimation (ALE) analysis to better understand the underlying neurophysiological mechanism of conscious processing of emotion in depression.
METHOD
Electronic databases were searched using the search terms "depression," "emotion recognition," and "neuroimaging" from inceptions to April 10th, 2023. We retrieved trials which explored the neuro-responses of depressive patients to explicit emotion recognition tasks. Two investigators independently performed literature selection, data extraction, and risk of bias assessment. The spatial consistency of brain activation in conscious facial expressions recognition was calculated using ALE. The robustness of the results was examined by Jackknife sensitivity analysis.
RESULTS
We retrieved 11,365 articles in total, 28 of which were included. In the overall analysis, we found increased activity in the middle temporal gyrus, superior temporal gyrus, parahippocampal gyrus, and cuneus, and decreased activity in the superior temporal gyrus, inferior parietal lobule, insula, and superior frontal gyrus. In response to positive stimuli, depressive patients showed hyperactivity in the medial frontal gyrus, middle temporal gyrus, and insula (uncorrected < 0.001). When receiving negative stimuli, a higher activation was found in the precentral gyrus, middle frontal gyrus, precuneus, and superior temporal gyrus (uncorrected < 0.001).
CONCLUSION
Among depressive patients, a broad spectrum of brain areas was involved in a deficit of conscious emotion processing. The activation of brain regions was different in response to positive or negative stimuli. Due to potential clinical heterogeneity, the findings should be treated with caution.
SYSTEMATIC REVIEW REGISTRATION
https://inplasy.com/inplasy-2022-11-0057/, identifier: 2022110057.
PubMed: 37448490
DOI: 10.3389/fpsyt.2023.1099426 -
Frontiers in Psychiatry 2023Ketamine and psychedelics have abuse liability. They can also induce "transformative experiences" where individuals experience enhanced states of awareness. This... (Review)
Review
BACKGROUND
Ketamine and psychedelics have abuse liability. They can also induce "transformative experiences" where individuals experience enhanced states of awareness. This enhanced awareness can lead to changes in preexisting behavioral patterns which could be beneficial in the treatment of substance use disorders (SUDs). Preclinical and clinical studies suggest that ketamine and psychedelics may alter markers associated with synaptic density, and that these changes may underlie effects such as sensitization, conditioned place preference, drug self-administration, and verbal memory performance. In this scoping review, we examined studies that measured synaptic markers in animals and humans after exposure to ketamine and/or psychedelics.
METHODS
A systematic search was conducted following PRISMA guidelines, through PubMed, EBSCO, Scopus, and Web of Science, based on a published protocol (Open Science Framework, DOI: 10.17605/OSF.IO/43FQ9). Both and studies were included. Studies on the following synaptic markers were included: dendritic structural changes, PSD-95, synapsin-1, synaptophysin-1, synaptotagmin-1, and SV2A.
RESULTS
Eighty-four studies were included in the final analyses. Seventy-one studies examined synaptic markers following ketamine treatment, nine examined psychedelics, and four examined both. Psychedelics included psilocybin/psilocin, lysergic acid diethylamide, N,N-dimethyltryptamine, 2,5-dimethoxy-4-iodoamphetamine, and ibogaine/noribogaine. Mixed findings regarding synaptic changes in the hippocampus and prefrontal cortex (PFC) have been reported when ketamine was administered in a single dose under basal conditions. Similar mixed findings were seen under basal conditions in studies that used repeated administration of ketamine. However, studies that examined animals during stressful conditions found that a single dose of ketamine counteracted stress-related reductions in synaptic markers in the hippocampus and PFC. Repeated administration of ketamine also counteracted stress effects in the hippocampus. Psychedelics generally increased synaptic markers, but results were more consistently positive for certain agents.
CONCLUSION
Ketamine and psychedelics can increase synaptic markers under certain conditions. Heterogeneous findings may relate to methodological differences, agents administered (or different formulations of the same agent), sex, and type of markers. Future studies could address seemingly mixed results by using meta-analytical approaches or study designs that more fully consider individual differences.
PubMed: 37435405
DOI: 10.3389/fpsyt.2023.1197890 -
Complex Psychiatry 2023Posttraumatic stress disorder (PTSD) is a complex multifactorial disorder influenced by the interaction of genetic and environmental factors. Analyses of epigenomic and... (Review)
Review
INTRODUCTION
Posttraumatic stress disorder (PTSD) is a complex multifactorial disorder influenced by the interaction of genetic and environmental factors. Analyses of epigenomic and transcriptomic modifications may help to dissect the biological factors underlying the gene-environment interplay in PTSD. To date, most human PTSD epigenetics studies have used peripheral tissue, and these findings have complex and poorly understood relationships to brain alterations. Studies examining brain tissue may help characterize the brain-specific transcriptomic and epigenomic profiles of PTSD. In this review, we compiled and integrated brain-specific molecular findings of PTSD from humans and animals.
METHODS
A systematic literature search according to the PRISMA criteria was performed to identify transcriptomic and epigenomic studies of PTSD, focusing on brain tissue from human postmortem samples or animal-stress paradigms.
RESULTS
Gene- and pathway-level convergence analyses revealed PTSD-dysregulated genes and biological pathways across brain regions and species. A total of 243 genes converged across species, with 17 of them significantly enriched for PTSD. Chemical synaptic transmission and signaling by G-protein-coupled receptors were consistently enriched across omics and species.
DISCUSSION
Our findings point out dysregulated genes highly replicated across PTSD studies in humans and animal models and suggest a potential role for the corticotropin-releasing hormone/orexin pathway in PTSD's pathophysiology. Further, we highlight current knowledge gaps and limitations and recommend future directions to address them.
PubMed: 37404872
DOI: 10.1159/000529536 -
Journal of Parkinson's Disease 2023Swallowing impairment, including altered physiology and aspiration, occur across the progression of Parkinson's disease (PD). The phase of respiration during which a... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Swallowing impairment, including altered physiology and aspiration, occur across the progression of Parkinson's disease (PD). The phase of respiration during which a swallow is initiated has been linked to swallowing impairment and aspiration in cohorts with dysphagia following stroke and head and neck cancer treatment, but has been understudied in PD. If similar findings are shown in individuals with PD, the implications for swallowing assessment and treatment are significant.
OBJECTIVE
The aim of this systematic review and meta-analysis of literature was to examine respiratory-swallow coordination measures and potential implications on swallowing physiology in individuals with PD.
METHODS
An extensive search of 7 databases (PubMed, EMBASE, Central, Web of Science, ProQuest Dissertations & Theses, Scopus, and CINAHL) with predetermined search terms was conducted. Inclusion criteria were individuals with PD and the use of objective evaluations of respiratory-swallow coordination.
RESULTS
Of the 13,760 articles identified, 11 met the inclusion criteria. This review supports the presence of atypical respiratory swallow patterning, respiratory pause duration and lung volume at swallow initiation in individuals with PD. The meta-analysis estimated an occurrence of 60% of non-expiration-expiration and 40% of expiration-expiration respiratory phase patterns surrounding swallowing.
CONCLUSION
Although this systematic review supports the occurrence of atypical respiratory-swallow coordination in individuals with PD, the evidence is limited by the variability in the methods of data acquisition, analysis, and reporting. Future research examining the impact of respiratory swallow coordination on swallowing impairment and airway protection using consistent, comparable, and reproducible methods and metrics in individuals with PD is warranted.
Topics: Humans; Parkinson Disease; Deglutition; Deglutition Disorders; Respiration
PubMed: 37393516
DOI: 10.3233/JPD-230057 -
Schizophrenia Bulletin Jan 2024Schizophrenia is highly heritable, with a polygenic effect of many genes conferring risk. Evidence on whether cumulative risk also predicts alterations in brain...
BACKGROUND AND HYPOTHESIS
Schizophrenia is highly heritable, with a polygenic effect of many genes conferring risk. Evidence on whether cumulative risk also predicts alterations in brain morphology and function is inconsistent. This systematic review examined evidence for schizophrenia polygenic risk score (sczPRS) associations with commonly used magnetic resonance imaging (MRI) measures. We expected consistent evidence to emerge for significant sczPRS associations with variation in structure and function, specifically in frontal, temporal, and insula cortices that are commonly implicated in schizophrenia pathophysiology.
STUDY DESIGN
In accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, we searched MEDLINE, Embase, and PsycINFO for peer-reviewed studies published between January 2013 and March 2022. Studies were screened against predetermined criteria and National Institutes of Health (NIH) quality assessment tools.
STUDY RESULTS
In total, 57 studies of T1-weighted structural, diffusion, and functional MRI were included (age range = 9-80 years, Nrange = 64-76 644). We observed moderate, albeit preliminary, evidence for higher sczPRS predicting global reductions in cortical thickness and widespread variation in functional connectivity, and to a lesser extent, region-specific reductions in frontal and temporal volume and thickness. Conversely, sczPRS does not predict whole-brain surface area or gray/white matter volume. Limited evidence emerged for sczPRS associations with diffusion tensor measures of white matter microstructure in a large community sample and smaller cohorts of children and young adults. These findings were broadly consistent across community and clinical populations.
CONCLUSIONS
Our review supports the hypothesis that schizophrenia is a disorder of disrupted within and between-region brain connectivity, and points to specific whole-brain and regional MRI metrics that may provide useful intermediate phenotypes.
Topics: Young Adult; Child; Humans; Adolescent; Adult; Middle Aged; Aged; Aged, 80 and over; Schizophrenia; Magnetic Resonance Imaging; Brain; Gray Matter; White Matter
PubMed: 37354489
DOI: 10.1093/schbul/sbad087 -
The Journal of Clinical Endocrinology... Dec 2023Polycystic ovary syndrome (PCOS) is a complex genetic trait and the most common endocrine disorder of women, clinically evident in 5% to 15% of reproductive-aged women...
PURPOSE
Polycystic ovary syndrome (PCOS) is a complex genetic trait and the most common endocrine disorder of women, clinically evident in 5% to 15% of reproductive-aged women globally, with associated cardiometabolic dysfunction. Adipose tissue (AT) dysfunction appears to play an important role in the pathophysiology of PCOS even in patients who do not have excess adiposity.
METHODS
We undertook a systematic review concerning AT dysfunction in PCOS, and prioritized studies that assessed AT function directly. We also explored therapies that targeted AT dysfunction for the treatment of PCOS.
RESULTS
Various mechanisms of AT dysfunction in PCOS were identified including dysregulation in storage capacity, hypoxia, and hyperplasia; impaired adipogenesis; impaired insulin signaling and glucose transport; dysregulated lipolysis and nonesterified free fatty acids (NEFAs) kinetics; adipokine and cytokine dysregulation and subacute inflammation; epigenetic dysregulation; and mitochondrial dysfunction and endoplasmic reticulum and oxidative stress. Decreased glucose transporter-4 expression and content in adipocytes, leading to decreased insulin-mediated glucose transport in AT, was a consistent abnormality despite no alterations in insulin binding or in IRS/PI3K/Akt signaling. Adiponectin secretion in response to cytokines/chemokines is affected in PCOS compared to controls. Interestingly, epigenetic modulation via DNA methylation and microRNA regulation appears to be important mechanisms underlying AT dysfunction in PCOS.
CONCLUSION
AT dysfunction, more than AT distribution and excess adiposity, contributes to the metabolic and inflammation abnormalities of PCOS. Nonetheless, many studies provided contradictory, unclear, or limited data, highlighting the urgent need for additional research in this important field.
Topics: Humans; Female; Adult; Polycystic Ovary Syndrome; Insulin Resistance; Phosphatidylinositol 3-Kinases; Adipose Tissue; Insulin; Cytokines; Obesity; Inflammation; Glucose
PubMed: 37329216
DOI: 10.1210/clinem/dgad356 -
PloS One 2023Variability in spine kinematics is a common motor adaptation to pain, which has been measured in various ways. However, it remains unclear whether low back pain (LBP) is...
BACKGROUND
Variability in spine kinematics is a common motor adaptation to pain, which has been measured in various ways. However, it remains unclear whether low back pain (LBP) is typically characterised by increased, decreased or unchanged kinematic variability. Therefore, the aim of this review was to synthesise the evidence on whether the amount and structure of spine kinematic variability is altered in people with chronic non-specific LBP (CNSLBP).
METHODS
Electronic databases, grey literature, and key journals were searched from inception up to August 2022, following a published and registered protocol. Eligible studies must investigated kinematic variability in CNSLBP people (adults ≥18 years) while preforming repetitive functional tasks. Two reviewers conducted screening, data extraction, and quality assessment independently. Data synthesis was conducted per task type and individual results were presented quantitatively to provide a narrative synthesis. The overall strength of evidence was rated using the Grading of Recommendations, Assessment, Development and Evaluation guidelines.
FINDINGS
Fourteen observational studies were included in this review. To facilitate the interpretation of the results, the included studies were grouped into four categories according to the task preformed (i.e., repeated flexion and extension, lifting, gait, and sit to stand to sit task). The overall quality of evidence was rated as a very low, primarily due to the inclusion criteria that limited the review to observational studies. In addition, the use of heterogeneous metrics for analysis and varying effect sizes contributed to the downgrade of evidence to a very low level.
INTERPRETATION
Individuals with chronic non-specific LBP exhibited altered motor adaptability, as evidenced by differences in kinematic movement variability during the performance of various repetitive functional tasks. However, the direction of the changes in movement variability was not consistent across studies.
Topics: Adult; Humans; Low Back Pain; Spine; Acclimatization; Benchmarking; Databases, Factual
PubMed: 37315096
DOI: 10.1371/journal.pone.0287029 -
Neuropsychology Review Jun 2024In recent years, there has been an increasing quest in improving our understanding of the neurocognitive deficits underlying adult attention-deficit/hyperactivity... (Meta-Analysis)
Meta-Analysis Review
In recent years, there has been an increasing quest in improving our understanding of the neurocognitive deficits underlying adult attention-deficit/hyperactivity disorder (ADHD). Current statistical manuals of psychiatric disorders emphasize inattention and hyperactivity-impulsivity symptoms, but empirical studies have also shown consistent alterations in inhibitory control. To date, there is no established neuropsychological test to assess inhibitory control deficits in adult ADHD. A common paradigm for assessing response inhibition is the stop-signal task (SST). Following PRISMA-selection criteria, our systematic review and meta-analysis integrated the findings of 26 publications with 27 studies examining the SST in adult ADHD. The meta-analysis, which included 883 patients with adult ADHD and 916 control participants, revealed reliable inhibitory control deficits, as expressed in prolonged SST response times, with a moderate effect size = 0.51 (95% CI: 0.376-0.644, < 0.0001). The deficits were not moderated by study quality, sample characteristics or clinical parameters, suggesting that they may be a phenotype in this disorder. The analyses of secondary outcome measures revealed greater SST omission errors and reduced go accuracy in patients, indicative of altered sustained attention. However, only few (N < 10) studies were available for these measures. Our meta-analysis suggests that the SST, in conjunction with other tests and questionnaires, could become a valuable tool for assessing inhibitory control deficits in adult ADHD.
Topics: Humans; Attention Deficit Disorder with Hyperactivity; Inhibition, Psychological; Adult; Neuropsychological Tests; Executive Function; Reaction Time
PubMed: 37300725
DOI: 10.1007/s11065-023-09592-5 -
Current Issues in Molecular Biology May 2023The gut microbiota is relatively stable; however, various factors can precipitate an imbalance that is known to be associated with various diseases. We aimed to conduct... (Review)
Review
BACKGROUND
The gut microbiota is relatively stable; however, various factors can precipitate an imbalance that is known to be associated with various diseases. We aimed to conduct a systematic literature review of studies reporting the effects of ionizing radiation on the composition, richness, and diversity of the gut microbiota of animals.
METHODS
A systematic literature search was performed in PubMed, EMBASE, and Cochrane library databases. The standard methodologies expected by Cochrane were utilized.
RESULTS
We identified 3531 non-duplicated records and selected twenty-nine studies after considering the defined inclusion criteria. The studies were found to be heterogeneous, with significant differences in the chosen populations, methodologies, and outcomes. Overall, we found evidence of an association between ionizing radiation exposure and dysbiosis, with a reduction of microbiota diversity and richness and alterations in the taxonomic composition. Although differences in taxonomic composition varied across studies, Proteobacteria, Verrucomicrobia, , and most consistently reported to be relatively more abundant after ionizing radiation exposure, whereas Bacteroidetes, Firmicutes, and were relatively reduced.
CONCLUSIONS
This review highlights the effect of ionizing exposure on gut microbiota diversity, richness, and composition. It paves the way for further studies on human subjects regarding gastrointestinal side effects in patients submitted to treatments with ionizing radiation and the development of potential preventive, therapeutic approaches.
PubMed: 37232718
DOI: 10.3390/cimb45050249