scholarly journals Associations and Heritability of Auditory Encoding, Gray Matter, and Attention in Schizophrenia

2018 ◽  
Vol 45 (4) ◽  
pp. 859-870 ◽  
Author(s):  
Yu-Han Chen ◽  
Breannan Howell ◽  
J Christopher Edgar ◽  
Mingxiong Huang ◽  
Peter Kochunov ◽  
...  

Abstract Background Auditory encoding abnormalities, gray-matter loss, and cognitive deficits are all candidate schizophrenia (SZ) endophenotypes. This study evaluated associations between and heritability of auditory network attributes (function and structure) and attention in healthy controls (HC), SZ patients, and unaffected relatives (UR). Methods Whole-brain maps of M100 auditory activity from magnetoencephalography recordings, cortical thickness (CT), and a measure of attention were obtained from 70 HC, 69 SZ patients, and 35 UR. Heritability estimates (h2r) were obtained for M100, CT at each group-difference region, and the attention measure. Results SZ patients had weaker bilateral superior temporal gyrus (STG) M100 responses than HC and a weaker right frontal M100 response than UR. Abnormally large M100 responses in left superior frontal gyrus were observed in UR and SZ patients. SZ patients showed smaller CT in bilateral STG and right frontal regions. Interrelatedness between 3 putative SZ endophenotypes was demonstrated, although in the left STG the M100 and CT function−structure associations observed in HC and UR were absent in SZ patients. Heritability analyses also showed that right frontal M100 and bilateral STG CT measures are significantly heritable. Conclusions Present findings indicated that the 3 SZ endophenotypes examined are not isolated markers of pathology but instead are connected. The pattern of auditory encoding group differences and the pattern of brain function−structure associations differ as a function of brain region, indicating the need for regional specificity when studying these endophenotypes, and with the presence of left STG function−structure associations in HC and UR but not in SZ perhaps reflecting disease-associated damage to gray matter that disrupts function−structure relationships in SZ.

2021 ◽  
Vol 15 ◽  
Author(s):  
Kelly Rootes-Murdy ◽  
Elaheh Zendehrouh ◽  
Vince D. Calhoun ◽  
Jessica A. Turner

Introduction: Individuals with schizophrenia have consistent gray matter reduction throughout the cortex when compared to healthy individuals. However, the reduction patterns vary based on the quantity (concentration or volume) utilized by study. The objective of this study was to identify commonalities between gray matter concentration and gray matter volume effects in schizophrenia.Methods: We performed both univariate and multivariate analyses of case/control effects on 145 gray matter images from 66 participants with schizophrenia and 79 healthy controls, and processed to compare the concentration and volume estimates.Results: Diagnosis effects in the univariate analysis showed similar areas of volume and concentration reductions in the insula, occipitotemporal gyrus, temporopolar area, and fusiform gyrus. In the multivariate analysis, healthy controls had greater gray matter volume and concentration additionally in the superior temporal gyrus, prefrontal cortex, cerebellum, calcarine, and thalamus. In the univariate analyses there was moderate overlap between gray matter concentration and volume across the entire cortex (r = 0.56, p = 0.02). The multivariate analyses revealed only low overlap across most brain patterns, with the largest correlation (r = 0.37) found in the cerebellum and vermis.Conclusions: Individuals with schizophrenia showed reduced gray matter volume and concentration in previously identified areas of the prefrontal cortex, cerebellum, and thalamus. However, there were only moderate correlations across the cortex when examining the different gray matter quantities. Although these two quantities are related, concentration and volume do not show identical results, and therefore, should not be used interchangeably in the literature.


Neurology ◽  
2017 ◽  
Vol 90 (3) ◽  
pp. e254-e260 ◽  
Author(s):  
Jennifer S. Graves ◽  
Roland G. Henry ◽  
Bruce A.C. Cree ◽  
Geralyn Lambert-Messerlian ◽  
Ruth M. Greenblatt ◽  
...  

ObjectiveTo determine if ovarian aging as measured by levels of anti-Müllerian hormone (AMH) is associated with pattern of multiple sclerosis (MS) progression in women.MethodsWomen with MS and healthy controls were included from a longitudinal research cohort with up to 10 years follow-up. Plasma AMH levels were measured by ELISA for baseline and years 3, 5, and 8–10. Mixed effects logistic and linear regression models were employed, with adjustments for age, disease duration, and other covariables as appropriate.ResultsAMH levels were similar (0.98-fold difference, 95% confidence interval [CI] 0.69–1.37, p = 0.87) in women with MS (n = 412, mean age 42.6 years) and healthy controls (n = 180, mean age 44 years). In a multivariable model of women with MS, including adjustments for age, body mass index, and disease duration, 10-fold lower AMH level was associated with 0.43-higher Expanded Disability Status Scale (EDSS) score (95% CI 0.15–0.70, p = 0.003), 0.25-unit worse MS Functional Composite z score (95% CI −0.40 to −0.10, p = 0.0015), and 7.44 mm3 lower cortical gray matter volume (95% CI −14.6 to −0.30; p = 0.041) at baseline. In a multivariable random-intercept–random-slope model using all observations over time, 10-fold decrease in AMH was associated with a 0.27 increase in EDSS (95% CI 0.11–0.43, p = 0.006) and 5.48 mm3 (95% CI 11.3–0.33, p = 0.065) and 4.55 mm3 (95% CI 9.33–0.23, p = 0.062) decreases in total gray and cortical gray matter, respectively.ConclusionAs a marker of ovarian aging, lower AMH levels were associated with greater disability and gray matter loss in women with MS independent of chronological age and disease duration.


Critical Care ◽  
2021 ◽  
Vol 25 (1) ◽  
Author(s):  
Maria C. Barbosa-Silva ◽  
Maiara N. Lima ◽  
Denise Battaglini ◽  
Chiara Robba ◽  
Paolo Pelosi ◽  
...  

AbstractInfectious diseases may affect brain function and cause encephalopathy even when the pathogen does not directly infect the central nervous system, known as infectious disease-associated encephalopathy. The systemic inflammatory process may result in neuroinflammation, with glial cell activation and increased levels of cytokines, reduced neurotrophic factors, blood–brain barrier dysfunction, neurotransmitter metabolism imbalances, and neurotoxicity, and behavioral and cognitive impairments often occur in the late course. Even though infectious disease-associated encephalopathies may cause devastating neurologic and cognitive deficits, the concept of infectious disease-associated encephalopathies is still under-investigated; knowledge of the underlying mechanisms, which may be distinct from those of encephalopathies of non-infectious cause, is still limited. In this review, we focus on the pathophysiology of encephalopathies associated with peripheral (sepsis, malaria, influenza, and COVID-19), emerging therapeutic strategies, and the role of neuroinflammation. Graphic abstract


2016 ◽  
Vol 30 (1) ◽  
pp. 77-86 ◽  
Author(s):  
Pekka Hautasaari ◽  
Andrej M. Savić ◽  
Otto Loberg ◽  
Eini Niskanen ◽  
Jaakko Kaprio ◽  
...  

2008 ◽  
Vol 63 (6) ◽  
pp. 550-556 ◽  
Author(s):  
Kiyoto Kasai ◽  
Hidenori Yamasue ◽  
Mark W. Gilbertson ◽  
Martha E. Shenton ◽  
Scott L. Rauch ◽  
...  

2013 ◽  
Vol 19 (12) ◽  
pp. 1088-1093 ◽  
Author(s):  
Eun-Young Lee ◽  
Suman Sen ◽  
Paul J. Eslinger ◽  
Daymond Wagner ◽  
Michele L. Shaffer ◽  
...  

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