Morphometry of the amygdala in schizophrenia and psychotic bipolar disorder

Mahon, Pamela B.; Lee, David S.; Trinh, Huong; Tward, Daniel J.; Miller, Michael I.; Younes, Laurent; Barta, Patrick E.; Ratnanather, J. Tilak

doi:10.1016/j.schres.2015.02.011

Cited by 28 publications

(21 citation statements)

References 28 publications

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“…SCZ patients were found to have lower gray matter volumes than BD‐P in the posterior hippocampus bilaterally, left dorsolateral prefrontal cortex (DLPFC), left cerebellum, as well as in the superior temporal gyrus, planum temporale, and several subregions of the amygdala . SCZ patients also had smaller bilateral cerebellar cortical volumes compared to BPAD patients and HC, while no significant differences were found between BD‐P and BD‐NP .…”

Section: Resultsmentioning

confidence: 90%

Biological aspects and candidate biomarkers for psychotic bipolar disorder: A systematic review

Buoli

Caldiroli

Melter

et al. 2016

Psychiatry Clin Neurosci

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Aim:We carried out a systematic review of the available literature about potential biomarkers of psychotic bipolar disorder (BD-P), a specific subset presenting worse outcome and greater risk of relapse than non-psychotic bipolar disorder (BD-NP). Methods:We searched the main psychiatric databases (PubMed, ISI Web of Knowledge, PsychInfo). Only original articles with the main topic of BD-P compared to schizophrenia/BD-NP/healthy controls (HC) written in English from 1994 to 2015 were included.Results: BD-P patients presented higher kynurenic acid levels in the cerebrospinal fluid, elevated antiSaccharomyces cerevisiae antibodies levels, and lower serum levels of dehydroepiandrosterone sulfate and progesterone than BD-NP/HC. Event-related potentials abnormalities have been identified in BD-P with respect to BD-NP. BD-P patients also presented bigger ventricles but similar hippocampal volumes compared to BD-NP/HC. Although the results are contrasting, some cognitive deficits seemed to be related to the psychotic dimension of bipolar affective disorder, such as impairment in verbal/logical memory, working memory, verbal and semantic fluency and executive functioning. Finally, polymorphisms of genes, such as NRG1, 5HTTLPR (s), COMT, DAOA and some chromosome regions (16p12 and 13q), were positively associated with BD-P. Conclusion:Data about the identification of specific biomarkers for BD-P are promising, but most of them have not yet been replicated. They could lead the clinicians to an early diagnosis and proper treatment, thus ameliorating outcome of BD-P and reducing the biological changes associated with a long duration of illness. Further studies with bigger samples are needed to detect more specific biological markers of the psychotic dimension of bipolar affective disorder.Key words: biomarkers, bipolar disorder, psychoneurobiology, psychopathology, psychotic symptoms. B IOLOGICAL MARKERS, AS indicators of a biological or a pathological state and as parameters that can be measured objectively, could provide a valuable support to the clinical decision-making process in many branches of medicine, including psychiatry. Several findings in the field of mood disorders could provide the background for the identification of potential specific and objective biomarkers, which could be an important aid to better understand the course of illness, the mechanisms of vulnerability and of disease expression.A recent paper describing the work of the Biomarkers Network from the International Society for Bipolar Disorders (ISBD-BIONET) cited neuroimaging and genetic findings in bipolar affective disorder (BPAD) (e.g. the loss of gray matter, the altered activation of anterior temporal, ventral prefrontal and subcortical regions in response to emotional stimuli, the identification of several potential candidate genes associated with increased risk for developing *Correspondence: Alice Caldiroli, MD, Department of Psychiatry, University of Milan, Fondazione IRCCS Ca' Granda, Ospedale Maggiore Policlinico, via Francesco Sforza ...

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Section: Resultsmentioning

confidence: 90%

Biological aspects and candidate biomarkers for psychotic bipolar disorder: A systematic review

Buoli

Caldiroli

Melter

et al. 2016

Psychiatry Clin Neurosci

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“…Despite several decades of extensive research, it has been challenging to define the key molecular pathways and corresponding etiologies of these diseases. During the last two decades, the use of advanced imaging techniques such as functional magnetic resonance imaging (fMRI), gamma synchrony, and mapping of scalp electrical activity have helped to identify SCZ and BD endophenotypes, including atrophy of the cingulate gyrus and dorsolateral prefrontal cortex, mainly in the left brain hemisphere (Bangalore et al, 2009;Bleich-Cohen et al, 2012;Cullen et al, 2006;Li et al, 2016;Mahon et al, 2015;Meda et al, 2008;Mwansisya et al, 2017;Narayanaswamy, Kalmady, Venkatasubramanian, & Gangadhar, 2015;Prasad & Keshavan, 2008;Rockstroh et al, 1998;Venkatasubramanian, Jayakumar, Gangadhar, & Keshavan, 2008a, 2008bWalter et al, 2003;Weiss et al, 2004;Williams et al, 2009). In fact, the loss or reversal of brain asymmetry/laterality is one of the most consistent observations that have eluded an understanding in neurodevelopmental diseases like SCZ and BD (Ho et al, 2017;Wang et al, 2014;Williams et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Aberrant transcriptomes and DNA methylomes define pathways that drive pathogenesis and loss of brain laterality/asymmetry in schizophrenia and bipolar disorder

Abdolmaleky

Gower

Wong

et al. 2018

American J of Med Genetics Pt B

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Although the loss of brain laterality is one of the most consistent modalities in schizophrenia (SCZ) and bipolar disorder (BD), its molecular basis remains elusive. Our limited previous studies indicated that epigenetic modifications are key to the asymmetric transcriptomes of brain hemispheres. We used whole-genome expression microarrays to profile postmortem brain samples from subjects with SCZ, psychotic BD [BD[+]] or non-psychotic BD [BD(−)], or matched controls (10/group) and performed whole-genome DNA methylation (DNAM) profiling of the same samples (3-4/group) to identify pathways associated with SCZ or BD[+] and genes/sites susceptible to epigenetic regulation. qRT-PCR and quantitative DNAM analysis were employed to validate findings in larger sample sets (35/group). Gene Set Enrichment Analysis (GSEA) demonstrated that BMP signaling and astrocyte and cerebral cortex development are significantly (FDR q < 0.25) coordinately upregulated in both SCZ and BD[+], and glutamate signaling and TGFβ signaling are significantly coordinately upregulated in SCZ. GSEA also indicated that collagens are downregulated in right versus left brain of controls, but not in SCZ or BD[+] patients. IngenuityPathway Analysis predicted that TGFB2 is an upstream regulator of these genes (p = .0012).While lateralized expression of TGFB2 in controls (p = .017) is associated with a corresponding change in DNAM (p ≤ .023), lateralized expression and DNAM of TGFB2 are absent in SCZ or BD. Loss of brain laterality in SCZ and BD corresponds to aberrant epigenetic regulation of TGFB2 and changes in TGFβ signaling, indicating potential avenues for disease prevention/ treatment. K E Y W O R D Sbrain asymmetry, DNA methylation, NR2E1, schizophrenia, TGFB2

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“…This level of granularity allows for more sensitive localization of differences in amygdala structure. For example analysis of three-dimensional amygdala structure is used in different neuropsychiatric conditions such as psychosis [Mahon et al, 2015], Alzheimer disease [Cavedo et al, 2011] and genetic conditions [Haas and Reiss, 2012]. Further, this analysis is used to explore brain and behavior correlations in clinical populations [Peng et al, 2014].…”

Section: Introductionmentioning

confidence: 99%

Sex differences in amygdala shape: Insights from Turner syndrome

Green

Fierro

Raman

et al. 2016

Human Brain Mapping

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Objective: Sex differences in the manifestation of psychiatric disorders, including anxiety disorders, are among the most prominent findings in psychiatry. The study of Turner syndrome (TS), caused by X-monosomy, has the potential to reveal mechanisms that underline male/female differences in neuropsychiatric disorders. The amygdala has been implicated in numerous neuropsychiatric disorders. Previous studies suggest an effect of TS on amygdala volume as well as on amygdala-related behaviors such as anxiety. Our objective is to investigate the amygdala shape in TS. Specifically, we tested whether amygdala enlargements in TS are localized to specific nuclei implicated in anxiety, such as the basomedial nucleus. Experimental design: We use a surface-based analytical modeling approach to contrast 41 pre-estrogen treatment girls with TS (mean age 8.6 ± 2.4) with 34 age-and sex-matched typically developing (TD) controls (mean age 8.0 ± 2.8). Anxiety symptoms were assessed using the Revised Children’s Manifest Anxiety Scale - 2 (RCMAS-2) in both groups. Principal observations: TS was associated with anomalous enlargement of the amygdala. Surface-based modeling revealed shape differences (increased radial-distances) in bilateral basal and basomedial nuclei within the basolateral complex. RCMAS-2 Total Anxiety t-score was significantly higher in participants with TS compared with TD controls (P = 0.012). Conclusions: Group differences in global amygdala volumes were driven by local morphological increases in areas that are critically involved in face emotion processing and anxiety. In the context of increased amygdala volumes in TS, our results also showed increased worry and social anxiety in young girls with TS compared with TD. Hum Brain Mapp 37:1593–1601, 2016.

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Morphometry of the amygdala in schizophrenia and psychotic bipolar disorder

Cited by 28 publications

References 28 publications

Biological aspects and candidate biomarkers for psychotic bipolar disorder: A systematic review

Biological aspects and candidate biomarkers for psychotic bipolar disorder: A systematic review

Aberrant transcriptomes and DNA methylomes define pathways that drive pathogenesis and loss of brain laterality/asymmetry in schizophrenia and bipolar disorder

Sex differences in amygdala shape: Insights from Turner syndrome

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