scholarly journals Callosal morphology in schizophrenia: what can shape tell us about function and illness?

2014 ◽  
Vol 204 (1) ◽  
pp. 9-11 ◽  
Author(s):  
Mark Walterfang ◽  
Dennis Velakoulis
Keyword(s):  
Corpus Callosum ◽  
Psychiatric Disorders ◽  
Microstructural Analysis ◽  
Brain Disorders ◽  
Cortical Regions ◽  
Brain Change

SummaryExamination of the corpus callosum provides a window to cortical brain change in brain disorders. Combining volumetric with microstructural analysis allows a greater understanding of the biology underpinning change, and examining callosal structure alongside the structure of the cortical regions it interconnects may allow us to understand the true significance of callosal change in psychiatric disorders.

scholarly journals Redundancy Circuits of the Commissural Pathways in Human and Rhesus Macaque Brains

2020 ◽  
Author(s):  
Zulfar Ghulam-Jelani ◽  
Jessica Barrios-Martinez ◽  
Aldo Eguiluz-Melendez ◽  
Ricardo Gomez ◽  
Yury Anania ◽  
...  
Keyword(s):  
Corpus Callosum ◽  
Human Brain ◽  
Rhesus Macaque ◽  
Anterior Commissure ◽  
Brain Disorders ◽  
Commissural Pathways ◽  
Commissural Pathway ◽  
Cortical Regions ◽  
Temporal Redundancy ◽  
First Time

AbstractIt has been hypothesized that the human brain has traded redundancy for efficiency, but the structural existence has not been identified to examine this claim. Here, we report three redundancy circuits of the commissural pathways in primate brains, namely the orbitofrontal, temporal, and occipital redundancy circuits of the anterior commissure and corpus callosum. Each redundancy circuit has two distinctly separated routes connecting a common pair of cortical regions. We mapped their trajectories in human and rhesus macaque brains using individual and population-averaged tractography. The dissection results confirmed the existence of these redundancy circuits connecting the orbitofrontal lobe, amygdala, and visual cortex. The volume analysis showed a significant reduction in the orbitofrontal and occipital redundancy circuits of the human brain, whereas the temporal redundancy circuit had a substantial organizational difference between the human and rhesus macaque. Our overall findings suggest that the human brain is more efficient in the commissural pathway, as shown by the significantly reduced volume of the anterior commissure which serves as the backup connections for the corpus callosum. This reduction of the redundancy circuit may explain why humans are more vulnerable to psychiatric brain disorders stemming from the corpus callosum compared to non-human primates.SignificanceWe report and describe the connection routes of three redundancy circuits of the commissural pathways in human and rhesus macaque brains and compare their volumes. Our tractography and dissection studies confirmed that the human brain has smaller redundancy circuits. This is the first time such redundancy circuits of the commissural pathways have been identified, and their differences quantified in human and rhesus macaque to verify the redundancy-efficiency tradeoff hypothesis. The findings provide new insight into the topological organization of the human brain and may help understand the circuit mechanism of brain disorders involving these pathways.

scholarly journals Shape Profile of Corpus Callosum As a Signature to Phenotype Different Dementia

2020 ◽  
Author(s):  
Sandhya Mangalore ◽  
Shiva Shanker Reddy Mukku ◽  
Sriharish Vankayalapati ◽  
Palanimuthu Thangaraju Sivakumar ◽  
Mathew Varghese
Keyword(s):  
Corpus Callosum ◽  
Frontotemporal Dementia ◽  
Corticobasal Degeneration ◽  
Lewy Body Dementia ◽  
Clinical History ◽  
The Body ◽  
Cortical Atrophy ◽  
Alzheimer Dementia ◽  
Geriatric Clinic ◽  
Cortical Regions

Abstract Background Phenotyping dementia is always a complex task for a clinician. There is a need for more practical biomarkers to aid clinicians. Objective The aim of the study is to investigate the shape profile of corpus callosum (CC) in different phenotypes of dementia. Materials and Methods Our study included patients who underwent neuroimaging in our facility as a part of clinical evaluation for dementia referred from Geriatric Clinic (2017–2018). We have analyzed the shape of CC and interpreted the finding using a seven-segment division. Results The sample included MPRAGE images of Alzheimer’ dementia (AD) (n = 24), posterior cortical atrophy- Alzheimer’ dementia (PCA-AD) (n = 7), behavioral variant of frontotemporal dementia (Bv-FTD) (n = 17), semantic variant frontotemporal dementia (Sv-FTD) (n = 11), progressive nonfluent aphasia (PNFA) (n = 4), Parkinson’s disease dementia (PDD) (n = 5), diffuse Lewy body dementia (n = 7), progressive supranuclear palsy (PSP) (n = 3), and corticobasal degeneration (CBD) (n = 3). We found in posterior dementias such as AD and PCA-AD that there was predominant atrophy of splenium of CC. In Bv-FTD, the genu and anterior half of the body of CC was atrophied, whereas in PNFA, PSP, PDD, and CBD there was atrophy of the body of CC giving a dumbbell like profile. Conclusion Our study findings were in agreement with the anatomical cortical regions involved in different phenotypes of dementia. Our preliminary study highlighted potential usefulness of CC in the clinical setting for phenotyping dementia in addition to clinical history and robust biomarkers.

Fatty acid composition of the postmortem corpus callosum of patients with schizophrenia, bipolar disorder, or major depressive disorder

2017 ◽  
Vol 39 ◽  
pp. 51-56 ◽  
Author(s):  
K. Hamazaki ◽  
M. Maekawa ◽  
T. Toyota ◽  
B. Dean ◽  
T. Hamazaki ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Bipolar Disorder ◽  
Major Depressive Disorder ◽  
Fatty Acid ◽  
White Matter ◽  
Corpus Callosum ◽  
Depressive Disorder ◽  
Psychiatric Disorders ◽  
Postmortem Brain ◽  
Major Depressive

AbstractBackgroundStudies investigating the relationship between n-3 polyunsaturated fatty acid (PUFA) levels and psychiatric disorders have thus far focused mainly on analyzing gray matter, rather than white matter, in the postmortem brain. In this study, we investigated whether PUFA levels showed abnormalities in the corpus callosum, the largest area of white matter, in the postmortem brain tissue of patients with schizophrenia, bipolar disorder, or major depressive disorder.MethodsFatty acids in the phospholipids of the postmortem corpus callosum were evaluated by thin-layer chromatography and gas chromatography. Specimens were evaluated for patients with schizophrenia (n = 15), bipolar disorder (n = 15), or major depressive disorder (n = 15) and compared with unaffected controls (n = 15).ResultsIn contrast to some previous studies, no significant differences were found in the levels of PUFAs or other fatty acids in the corpus callosum between patients and controls. A subanalysis by sex gave the same results. No significant differences were found in any PUFAs between suicide completers and non-suicide cases regardless of psychiatric disorder diagnosis.ConclusionsPatients with psychiatric disorders did not exhibit n-3 PUFAs deficits in the postmortem corpus callosum relative to the unaffected controls, and the corpus callosum might not be involved in abnormalities of PUFA metabolism. This area of research is still at an early stage and requires further investigation.

The frontal aging hypothesis evaluated

2000 ◽  
Vol 6 (6) ◽  
pp. 705-726 ◽  
Author(s):  
PAMELA M. GREENWOOD
Keyword(s):  
Cognitive Aging ◽  
Functional Decline ◽  
Frontal Lobes ◽  
Age Related ◽  
Conflicting Evidence ◽  
Frontal Lobe Function ◽  
Volume Blood ◽  
Cortical Regions ◽  
Effects Of Aging ◽  
Brain Change

That the human frontal lobes are particularly vulnerable to age-related deterioration has been frequently invoked as an explanation of functional decline in aging. This “frontal aging hypothesis” is evaluated in this review by examining evidence of selectively reduced frontal lobe function in aging. The frontal aging hypothesis predicts that functions largely dependent on frontal regions would decline in aging, while functions largely independent of frontal lobes would remain relatively spared. The hypothesis further predicts that age-related brain change would selectively impact frontal regions. The literatures on working memory, visuospatial attention, face recognition, and implicit memory were reviewed as exemplars of functions dependent on prefrontal, parietal, temporal and occipitotemporal cortices, respectively, with a view to establishing mediating structures and effects of aging. Age sensitivity was seen both in functions dependent on frontal integrity as well as in functions apparently independent of frontal integrity. Further, although prefrontal areas exhibit age-related decreases in regional volume, blood flow and metabolism, nonfrontal cortical regions undergo similar declines. It is concluded that while the frontal lobes are subject to age-related changes reflected in both behavior and pathology, there is only weak and conflicting evidence that frontal regions are selectively and differentially affected by aging. It is argued that a network-based theory of cognitive aging has advantages over the localizationist approach inherent in the frontal aging hypothesis. (JINS, 2000, 6, 705–726.)

scholarly journals Analysis of shared heritability in common disorders of the brain

Science ◽  
2018 ◽  
Vol 360 (6395) ◽  
pp. eaap8757 ◽  
Author(s):  
◽  
Verneri Anttila ◽  
Brendan Bulik-Sullivan ◽  
Hilary K. Finucane ◽  
Raymond K. Walters ◽  
...  
Keyword(s):  
Psychiatric Disorders ◽  
Neurological Disorders ◽  
Statistical Power ◽  
Association Studies ◽  
Genetic Correlations ◽  
Genome Wide Association Studies ◽  
Brain Disorders ◽  
Cognitive Measures ◽  
Genome Wide ◽  
The Brain

Disorders of the brain can exhibit considerable epidemiological comorbidity and often share symptoms, provoking debate about their etiologic overlap. We quantified the genetic sharing of 25 brain disorders from genome-wide association studies of 265,218 patients and 784,643 control participants and assessed their relationship to 17 phenotypes from 1,191,588 individuals. Psychiatric disorders share common variant risk, whereas neurological disorders appear more distinct from one another and from the psychiatric disorders. We also identified significant sharing between disorders and a number of brain phenotypes, including cognitive measures. Further, we conducted simulations to explore how statistical power, diagnostic misclassification, and phenotypic heterogeneity affect genetic correlations. These results highlight the importance of common genetic variation as a risk factor for brain disorders and the value of heritability-based methods in understanding their etiology.

scholarly journals Genetic Identification of Cell Types Underlying Brain Complex Traits Yields Novel Insights Into the Etiology of Parkinson’s Disease

2019 ◽  
Author(s):  
Julien Bryois ◽  
Nathan G. Skene ◽  
Thomas Folkmann Hansen ◽  
Lisette J.A. Kogelman ◽  
Hunna J. Watson ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Psychiatric Disorders ◽  
Complex Traits ◽  
Cell Types ◽  
Genetic Identification ◽  
Genome Wide Association Studies ◽  
Brain Disorders ◽  
Disease Etiology ◽  
Transcriptomic Data

AbstractGenome-wide association studies (GWAS) have discovered hundreds of loci associated with complex brain disorders, and provide the best current insights into the etiology of these idiopathic traits. However, it remains unclear in which cell types these variants may be active, which is essential for understanding disease etiology and for disease modelling. Here we integrate GWAS results with single-cell transcriptomic data from the entire nervous system to systematically identify cell types underlying psychiatric disorders, neurological conditions, and other brain complex traits. We show that psychiatric disorders are predominantly associated with excitatory neurons from the cortex/hippocampus, medium spiny neurons from the striatum, diverse sets of midbrain neurons, and inhibitory neurons from the cortex/hippocampus. Cognitive traits were generally associated with similar cell types but their associations were driven by different genes. Neurological disorders were associated with different cell types, consistent with other lines of evidence. Notably, we found that Parkinson’s disease is not only genetically associated with dopaminergic neurons but also with serotonergic neurons and cells from the oligodendrocyte lineage. Using post-mortem brain transcriptomic data, we confirmed alterations in these cells, even at the earliest stages of disease progression. Altogether, our study provides a solid framework for understanding the cellular basis of complex brain disorders and reveals a new unexpected role of oligodendrocytes in Parkinson’s disease.

scholarly journals Opportunities and limitations of genetically modified nonhuman primate models for neuroscience research

2020 ◽  
Vol 117 (39) ◽  
pp. 24022-24031 ◽  
Author(s):  
Guoping Feng ◽  
Frances E. Jensen ◽  
Henry T. Greely ◽  
Hideyuki Okano ◽  
Stefan Treue ◽  
...  
Keyword(s):  
Human Brain ◽  
Psychiatric Disorders ◽  
Nonhuman Primate ◽  
Genetically Modified ◽  
Brain Disorders ◽  
Neuroscience Research ◽  
Circuit Formation ◽  
The Impact

The recently developed new genome-editing technologies, such as the CRISPR/Cas system, have opened the door for generating genetically modified nonhuman primate (NHP) models for basic neuroscience and brain disorders research. The complex circuit formation and experience-dependent refinement of the human brain are very difficult to model in vitro, and thus require use of in vivo whole-animal models. For many neurodevelopmental and psychiatric disorders, abnormal circuit formation and refinement might be at the center of their pathophysiology. Importantly, many of the critical circuits and regional cell populations implicated in higher human cognitive function and in many psychiatric disorders are not present in lower mammalian brains, while these analogous areas are replicated in NHP brains. Indeed, neuropsychiatric disorders represent a tremendous health and economic burden globally. The emerging field of genetically modified NHP models has the potential to transform our study of higher brain function and dramatically facilitate the development of effective treatment for human brain disorders. In this paper, we discuss the importance of developing such models, the infrastructure and training needed to maximize the impact of such models, and ethical standards required for using these models.

Concluding discussion

2019 ◽  
pp. 177-180
Author(s):  
Risto Näätänen ◽  
Teija Kujala ◽  
Gregory Light
Keyword(s):  
Cognitive Decline ◽  
Vegetative State ◽  
Persistent Vegetative State ◽  
Brain Disorders ◽  
Objective Monitoring ◽  
Age Related ◽  
Clinical Conditions ◽  
Age Related Cognitive Decline ◽  
Brain Change ◽  
Recovery Of Consciousness

This chapter looks at potential common underlying factors linking MMN/MMNm deficiency to the broad range of heterogeneous clinical conditions outlined in the book. Several promising clinical applications of MMN/MMNm are summarized, including the prediction of conversion to psychosis among clinically at-risk individuals, the prediction of the recovery of consciousness and cognitive capabilities in patients in a comatose or persistent vegetative state, the early detection of perceptual deficits in developmental brain disorders, and the early identification of the presence of Mild Cognitive Impairment (MCI). Furthermore, the evaluation of the cognitive decline occurring in different brain disorders, as well as the prediction of cognitive recovery after the occurrence of a stroke or other brain injury, and the objective monitoring of age-related cognitive brain change and potential countermeasures to slow down this age-related cognitive decline are discussed.

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