Reductions of grey matter volume in subjects at high risk of schizophrenia

NeuroImage ◽  
2001 ◽  
Vol 13 (6) ◽  
pp. 1118 ◽  
Author(s):  
S.L. Yates ◽  
H.C. Whalley ◽  
P. Miller ◽  
J.J.K. Best ◽  
D.C. Owens ◽  
...  
2014 ◽  
Vol 44 (16) ◽  
pp. 3491-3501 ◽  
Author(s):  
G. Modinos ◽  
P. Allen ◽  
M. Frascarelli ◽  
S. Tognin ◽  
L. Valmaggia ◽  
...  

Background.The majority of people at ultra high risk (UHR) of psychosis also present with co-morbid affective disorders such as depression or anxiety. The neuroanatomical and clinical impact of UHR co-morbidity is unknown.Method.We investigated group differences in grey matter volume using baseline magnetic resonance images from 121 participants in four groups: UHR with depressive or anxiety co-morbidity; UHR alone; major depressive disorder; and healthy controls. The impact of grey matter volume on baseline and longitudinal clinical/functional data was assessed with regression analyses.Results.The UHR-co-morbidity group had lower grey matter volume in the anterior cingulate cortex than the UHR-alone group, with an intermediate effect between controls and patients with major depressive disorder. In the UHR-co-morbidity group, baseline anterior cingulate volume was negatively correlated with baseline suicidality/self-harm and obsessive–compulsive disorder symptoms.Conclusions.Co-morbid depression and anxiety disorders contributed distinctive grey matter volume reductions of the anterior cingulate cortex in people at UHR of psychosis. These volumetric deficits were correlated with baseline measures of depression and anxiety, suggesting that co-morbid depressive and anxiety diagnoses should be carefully considered in future clinical and imaging studies of the psychosis high-risk state.


2011 ◽  
Vol 21 ◽  
pp. S63-S64 ◽  
Author(s):  
J.M. Stone ◽  
S. Bhattacharyya ◽  
G. Barker ◽  
P.K. McGuire

2016 ◽  
Vol 173 (3) ◽  
pp. 152-158 ◽  
Author(s):  
Vanessa L. Cropley ◽  
Ashleigh Lin ◽  
Barnaby Nelson ◽  
Renate L.E.P. Reniers ◽  
Alison R. Yung ◽  
...  

2013 ◽  
Vol 23 ◽  
pp. S274-S275
Author(s):  
G. Sugranyes ◽  
E. De la Serna ◽  
C. Espelt ◽  
A. Calvo ◽  
V. Sanchez-Gistau ◽  
...  

2013 ◽  
Vol 44 (3) ◽  
pp. 489-498 ◽  
Author(s):  
S. Tognin ◽  
A. Riecher-Rössler ◽  
E. M. Meisenzahl ◽  
S. J. Wood ◽  
C. Hutton ◽  
...  

BackgroundGrey matter volume and cortical thickness represent two complementary aspects of brain structure. Several studies have described reductions in grey matter volume in people at ultra-high risk (UHR) of psychosis; however, little is known about cortical thickness in this group. The aim of the present study was to investigate cortical thickness alterations in UHR subjects and compare individuals who subsequently did and did not develop psychosis.MethodWe examined magnetic resonance imaging data collected at four different scanning sites. The UHR subjects were followed up for at least 2 years. Subsequent to scanning, 50 UHR subjects developed psychosis and 117 did not. Cortical thickness was examined in regions previously identified as sites of neuroanatomical alterations in UHR subjects, using voxel-based cortical thickness.ResultsAt baseline UHR subjects, compared with controls, showed reduced cortical thickness in the right parahippocampal gyrus (p < 0.05, familywise error corrected). There were no significant differences in cortical thickness between the UHR subjects who later developed psychosis and those who did not.ConclusionsThese data suggest that UHR symptomatology is characterized by alterations in the thickness of the medial temporal cortex. We did not find evidence that the later progression to psychosis was linked to additional alterations in cortical thickness, although we cannot exclude the possibility that the study lacked sufficient power to detect such differences.


Author(s):  
William D. Hopkins ◽  
Cheryl D. Stimpson ◽  
Chet C. Sherwood

Bonobos and chimpanzees are two closely relates species of the genus Pan, yet they exhibit marked differences in anatomy, behaviour and cognition. For this reason, comparative studies on social behaviour, cognition and brain organization between these two species provide important insights into evolutionary models of human origins. This chapter summarizes studies on socio-communicative competencies and social cognition in chimpanzees and bonobos from the authors’ laboratory in comparison to previous reports. Additionally, recent data on species differences and similarities in brain organization in grey matter volume and distribution is presented. Some preliminary findings on microstructural brain organization such as neuropil space and cellular distribution in key neurotransmitters and neuropeptides involved in social behaviour and cognition is presented. Though these studies are in their infancy, the findings point to potentially important differences in brain organization that may underlie bonobo and chimpanzees’ differences in social behaviour, communication and cognition. Les bonobos et les chimpanzés sont deux espèces du genus Pan prochement liées, néanmoins ils montrent des différences anatomiques, comportementales et cognitives marquées. Pour cette raison, les études comparatives sur le comportement social, la cognition et l’organisation corticale entre ces deux espèces fournissent des idées sur les modèles évolutionnaires des origines humaines. Dans ce chapitre, nous résumons des études sur les compétences socio-communicatives et la cognition sociale chez les chimpanzés et les bonobos de notre laboratoire en comparaison avec des rapports précédents. En plus, nous présentons des données récentes sur les différences et similarités d’organisation corticale du volume et distribution de la matière grise entre espèces. Nous présentons plus de résultats préliminaires sur l’organisation corticale microstructurale comme l’espace neuropile et la division cellulaire dans des neurotransmetteurs clés et les neuropeptides impliqués dans le comportement social et la cognition. Bien que ces études sont dans leur enfance, les résultats montrent des différences d’organisation corticale importantes qui sont à la base des différences de comportement social, la communication et la cognition entre les bonobos et les chimpanzés.


2021 ◽  
pp. jnnp-2020-323541
Author(s):  
Jessica L Panman ◽  
Vikram Venkatraghavan ◽  
Emma L van der Ende ◽  
Rebecca M E Steketee ◽  
Lize C Jiskoot ◽  
...  

ObjectiveProgranulin-related frontotemporal dementia (FTD-GRN) is a fast progressive disease. Modelling the cascade of multimodal biomarker changes aids in understanding the aetiology of this disease and enables monitoring of individual mutation carriers. In this cross-sectional study, we estimated the temporal cascade of biomarker changes for FTD-GRN, in a data-driven way.MethodsWe included 56 presymptomatic and 35 symptomatic GRN mutation carriers, and 35 healthy non-carriers. Selected biomarkers were neurofilament light chain (NfL), grey matter volume, white matter microstructure and cognitive domains. We used discriminative event-based modelling to infer the cascade of biomarker changes in FTD-GRN and estimated individual disease severity through cross-validation. We derived the biomarker cascades in non-fluent variant primary progressive aphasia (nfvPPA) and behavioural variant FTD (bvFTD) to understand the differences between these phenotypes.ResultsLanguage functioning and NfL were the earliest abnormal biomarkers in FTD-GRN. White matter tracts were affected before grey matter volume, and the left hemisphere degenerated before the right. Based on individual disease severities, presymptomatic carriers could be delineated from symptomatic carriers with a sensitivity of 100% and specificity of 96.1%. The estimated disease severity strongly correlated with functional severity in nfvPPA, but not in bvFTD. In addition, the biomarker cascade in bvFTD showed more uncertainty than nfvPPA.ConclusionDegeneration of axons and language deficits are indicated to be the earliest biomarkers in FTD-GRN, with bvFTD being more heterogeneous in disease progression than nfvPPA. Our data-driven model could help identify presymptomatic GRN mutation carriers at risk of conversion to the clinical stage.


2020 ◽  
Author(s):  
A. Buhrmann ◽  
A. M. A. Brands ◽  
J. van der Grond ◽  
C. Schilder ◽  
R. C. van der Mast ◽  
...  

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