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Publication
Featured researches published by Carissa Nadia Kuswanto.
Journal of Neural Transmission | 2013
Qian Jun Yap; Irvin Teh; Paolo Fusar-Poli; Min Yi Sum; Carissa Nadia Kuswanto; Kang Sim
Delineating the normal development of brain white matter (WM) over the human lifespan is crucial to improved understanding of underlying WM pathology in neuropsychiatric and neurological conditions. We review the extant literature concerning diffusion tensor imaging studies of brain WM development in healthy individuals available until October 2012, summarise trends of normal development of human brain WM and suggest possible future research directions. Temporally, brain WM maturation follows a curvilinear pattern with an increase in fractional anisotropy (FA) from newborn to adolescence, decelerating in adulthood till a plateau around mid-adulthood, and a more rapid decrease of FA from old age onwards. Spatially, brain WM tracts develop from central to peripheral regions, with evidence of anterior-to-posterior maturation in commissural and projection fibres. The corpus callosum and fornix develop first and decline earlier, whilst fronto-temporal WM tracts like cingulum and uncinate fasciculus have protracted maturation and decline later. Prefrontal WM is most vulnerable with greater age-related FA reduction compared with posterior WM. Future large scale studies adopting longitudinal design will better clarify human brain WM changes over time.
Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology | 2012
Carissa Nadia Kuswanto; Irvin Teh; Tih-Shih Lee; Kang Sim
Earlier structural magnetic resonance imaging in schizophrenia have noted smaller white matter volumes in diverse brain regions and recent diffusion tensor imaging (DTI) studies have allowed better elucidation of changes in brain white matter integrity within the illness. As white matter abnormalities have been reported to occur early in the course of schizophrenia, we systematically review extant DTI studies of anomalies of white matter integrity in first episode schizophrenia (FES) up till October 2011. Overall, disruptions of white matter integrity were found in the cortical, subcortical brain regions and white matter associative and commissural tracts, suggesting that changes of cortical-subcortical white matter integrity were found at an early stage of the disorder. These changes in white matter integrity were correlated with specific cognitive deficits (verbal and spatial working memory) as well as psychopathology (positive more than negative symptoms) in patients with FES. The correlation of these white matter integrity changes with cognitive and phenomenological factors may shed light on neurobiological substrates underlying these clinical manifestations. Future studies need to validate these findings in larger samples of subjects and in different populations as well as chart the progress of these cerebral white matter changes over time so as to better appreciate their trajectory with illness course, treatment and chronicity.
American Journal of Medical Genetics | 2012
Carissa Nadia Kuswanto; Puay-San Woon; Xuebin Zheng; Anqi Qiu; Yih-Yian Sitoh; Yiong Huak Chan; Jianjun Liu; Hywel Williams; Wei Yi Ong; Kang Sim
Genome‐wide association, case association genetic and meta‐analytic studies have highlighted ZNF804A as a robust genome‐wide supported susceptibility gene for schizophrenia (SCZ). In view of the possible involvement of ZNF804A gene in early neurodevelopment and cellular processes including oligodendrocyte proliferation and differentiation, we examined the effect of ZNF804A on brain WM (WM) integrity in patients with SCZ. Based on extant data in healthy controls (HC), we hypothesized that ZNF804A risk variant rs1344706 is associated with lower fractional anisotropy (FA) in brain regions within cortico‐limbic circuits, namely frontal, parietal, medial temporal lobes, and cingulate gyri in SCZ. A total of 200 Chinese participants (125 patients with DSM‐IV diagnosis of SCZ and 75 controls) were genotyped using blood samples, a subset of 153 participants (89 patients with DSM‐IV diagnosis of SCZ and 64 controls) underwent structural magnetic resonance imaging and diffusion tensor imaging (DTI). There are significant effects of diagnosis (left cingulate gyrus: Adjusted F1,149 = 9.36, P = 0.003) and diagnosis–genotype interactions (left parietal lobe: Adjusted F1,147 = 7.39, P = 0.007; right parietal lobe: Adjusted F1,147 = 6.95, P = 0.009; right medial temporal lobe: Adjusted F1,147 = 8.79, P = 0.004; left cingulate gyrus: Adjusted F1,147 = 8.02, P = 0.005). Specifically, we found that patients with SCZ who are risk T homozygotes have lower FA in bilateral parietal lobes, and left cingulate gyrus compared with G carriers. Compared with risk T homozygotes in HC, patients with SCZ who are risk T homozygotes have decreased FA in bilateral parietal lobes, and left cingulate gyrus as well as right medial temporal lobe. Our findings suggest that ZNF804A risk variant influence WM integrity involving cortico‐limbic brain regions in SCZ and highlight the importance of investigating the impact of genome‐wide supported risk factors on intermediate phenotypes with potential to shed light on the neurobiology of SCZ.
British Journal of Psychiatry | 2014
Simon L. Collinson; Swu Chyi Gan; Puay San Woon; Carissa Nadia Kuswanto; Min Yi Sum; Guo Liang Yang; Ji Min Lui; Yih Yian Sitoh; Wieslaw L. Nowinski; Kang Sim
BACKGROUND Abnormalities in the corpus callosum have been reported in patients with schizophrenia for over 30 years but the influence of inter-individual differences and illness characteristics remains to be fully elucidated. AIMS To examine the influence of individual and illness characteristics on the corpus callosum in Chinese Singaporean patients with schizophrenia. METHOD Using magnetic resonance and diffusion tensor imaging, mean corpus callosum area, volume and fractional anisotropy were investigated in 120 Chinese Singaporean patients (52 with chronic and 68 with first-episode schizophrenia) and compared with data from 75 matched healthy controls. RESULTS Both area and volume were significantly reduced in patients relative to controls but no significant differences in corpus callosum existed between genders in either patients or controls. Differences in area and volume of the corpus callosum were greatest in patients whose condition was chronic relative to patients with a first episode and controls. Anterior callosum in patients, regardless of chronicity, was no different to that of controls. CONCLUSIONS Morphological abnormalities in the corpus callosum may increase with illness progression.
PLOS ONE | 2012
Muhammad Farid Abdul-Rahman; Anqi Qiu; Puay San Woon; Carissa Nadia Kuswanto; Simon L. Collinson; Kang Sim
Disruption of fronto-temporal connections involving the arcuate fasciculus (AF) may underlie language processing anomalies and psychotic features such as auditory hallucinations in schizophrenia. No study to date has specifically investigated abnormalities of white matter integrity at particular loci along the AF as well as its regional lateralization in schizophrenia. We examined white matter changes (fractional anisotropy (FA), axial diffusivity (AD), asymmetry indices) along the whole extent of the AF and their relationship with psychotic symptoms in 32 males with schizophrenia and 44 healthy males. Large deformation diffeomorphic metric mapping and Fiber Assignment Continuous Tracking were employed to characterize FA and AD along the geometric curve of the AF. Our results showed that patients with schizophrenia had lower FA in the frontal aspects of the left AF compared with healthy controls. Greater left FA and AD lateralization in the temporal segment of AF were associated with more severe positive psychotic symptoms such as delusions and hallucinations in patients with schizophrenia. Disruption of white matter integrity of the left frontal AF and accentuation of normal left greater than right asymmetry of FA/AD in the temporal AF further support the notion of aberrant fronto-temporal connectivity in schizophrenia. AF pathology can affect corollary discharge of neural signals from frontal speech/motor initiation areas to suppress activity of auditory cortex that may influence psychotic phenomena such as auditory hallucinations and facilitate elaboration of delusional content.
Journal of Neural Transmission | 2011
Yoanna Arlina Kurnianingsih; Carissa Nadia Kuswanto; Roger S. McIntyre; Anqi Qiu; Beng-Choon Ho; Kang Sim
Studies examining intermediate phenotypes such as neurocognitive and neuroanatomical measures along with susceptibility genes are important for improving our understanding of the neural basis of schizophrenia (SZ) and bipolar disorder (BD). In this paper, we review extant studies involving neurocognitive-genetic and neuroimaging-genetic perspectives and particularly related to catechol-O-methyltransferase (COMT), brain-derived neurotrophic factor (BDNF) and neuregulin-1 (NRG1) genes in SZ and BD. In terms of neurocognitive-genetic investigations, COMT and BDNF are the two most studied candidate genes especially in patients with SZ. Whereas BDNF Met carriers perform worse on verbal working memory, problem solving and visuo-spatial abilities, COMT Met carriers perform better in working memory, attention, executive functioning with evidence of genotype by diagnosis interactions including high-risk individuals. In terms of genetic-structural MRI studies, patients with SZ are found to have reductions in the frontal, temporal, parietal cortices, and limbic regions, which are associated with BDNF, COMT, and NRGI genes. Genetic-functional MRI studies in psychotic disorders are sparse, especially with regard to BD. These neurocognitive and neuroimaging findings are associated with genes which are implicated in functional pathways related to neuronal signaling, inter-neuronal communication and neuroplasticity.
American Journal of Medical Genetics | 2015
Carissa Nadia Kuswanto; Min Yi Sum; Anqi Qiu; Yih-Yian Sitoh; Jianjun Liu; Kang Sim
Although genome wide association studies have highlighted MicroRNA 137 (MIR137) as a novel susceptibility gene for schizophrenia, the mechanisms by which MIR137 risk variants mediate the neurobiology of schizophrenia are not clear. Based on extant data linking MIR 137 gene with structural brain anomalies and functional brain activations in schizophrenia, we hypothesized that MIR137 risk variants rs1625579 and rs1198588 would be associated with reduced fractional anisotropy in frontostriatal brain regions, impaired neurocognitive functioning and worse psychotic symptoms in schizophrenia patients compared with healthy controls. A total of 147 Chinese participants (84 patients with DSM‐IV diagnosis of schizophrenia (SCZ) and 63 healthy controls (HC)) were genotyped using blood samples and underwent diffusion tensor imaging. Neurocognitive domains and psychotic symptoms were assessed using The Brief Assessment of Cognition Battery for Schizophrenia and Positive and Negative Syndrome Scale respectively. We found significant diagnosis‐genotype interactions in the right orbitofrontal regions (rs1625579: F = 5.44, P = 0.021; rs1198599: F = 7.55, P = 0.005), left striatum (rs1625579: F = 8.09, P = 0.007; rs1198599: F = 9.56, P = 0.002), and negative symptoms (rs1625579: t = 2.45, P = 0.016; rs1198588: t = 2.29, P = 0.024). Specifically, SCZ carrying the risk TT genotype had worse negative symptoms and decreased FA in the fronto‐striatal regions compared to G and A allele carriers for rs1625579 and rs1198588 respectively, and worse attention and processing speed compared with G‐allele for rs1625579. Our findings suggested that the MI137 risk variants were associated with decreased fronto‐striatal brain white matter integrity which may underlie poorer attention, processing speed, and greater negative symptoms in schizophrenia.
Neuroscience & Biobehavioral Reviews | 2016
Carissa Nadia Kuswanto; Rowena Chin; Min Yi Sum; Somnath Sengupta; Andrea Fagiolini; Roger S. McIntyre; Eduard Vieta; Kang Sim
Recent data from genetic and brain imaging studies have urged rethinking of bipolar disorder (BD) and schizophrenia (SCZ) as lying along a continuum of major endogenous psychoses rather than dichotomous disorders. We systematically reviewed extant studies (from January 2000 to July 2015) that directly compared neurocognitive impairments in adults with SCZ and BD. Within 36 included studies, comparable neurocognitive impairments were found in SCZ and BD involving executive functioning, working memory, verbal fluency and motor speed. The extent and severity of neurocognitive impairments in patients with schizoaffective disorder, and BD with psychotic features occupy positions intermediate between SCZ and BD without psychotic features, suggesting spectrum of neurocognitive impairments across psychotic spectrum conditions. Neurocognitive impairments correlated with socio-demographic (lower education), clinical (more hospitalizations, longer duration of illness, negative psychotic symptoms and non-remission status), treatment (antipsychotics, anti-cholinergics) variables and lower psychosocial functioning. The convergent neurocognitive findings in both conditions support a continuum concept of psychotic disorders and further research is needed to clarify common and dissimilar progression of specific neurocognitive impairments longitudinally.
The Journal of Clinical Psychiatry | 2014
Puay San Woon; Min Yi Sum; Carissa Nadia Kuswanto; Guo Liang Yang; Yih Yian Sitoh; Tuck Wah Soong; Tih-Shih Lee; Wieslaw L. Nowinski; Kang Sim
OBJECTIVE Recent genomewide association studies have implicated the calcium channel, voltage-dependent, L type, alpha 1C subunit (CACNA1C) genetic variant in schizophrenia, which is associated with functional brain changes and cognitive deficits in healthy individuals. However, the impact of CACNA1C on brain white matter integrity in schizophrenia remains unclear. On the basis of prior evidence of CACNA1C-mediated changes involving cortical brain regions, we hypothesize that CACNA1C risk variant rs1006737 is associated with reductions of white matter integrity in the frontal, parietal, and temporal regions and cingulate gyrus. METHOD A total of 160 Chinese participants (96 DSM-IV-diagnosed patients with schizophrenia and 64 healthy controls) were genotyped by using blood samples and underwent structural magnetic resonance imaging and diffusion tensor imaging scans from 2008 to 2012. Two-way analysis of covariance was employed to examine CACNA1C-related genotype effects, diagnosis effects, and genotype × diagnosis interaction effects on fractional anisotropy (FA) of relevant brain regions. RESULTS Significant diagnosis-genotype interactions were observed (left frontal lobe mean FA: F₁,₁₅₆ = 6.22, P = .014; left parietal lobe mean FA: F₁,₁₅₆ = 7.14, P = .008; left temporal lobe mean FA: F₁,₁₅₆ = 8.37, P = .004). Compared with patients who were A carriers, patients who were G homozygotes had lower mean FA in the left frontal lobe (F₁,₉₃ = 2.504, P = .014), left parietal lobe (F₁,₉₃ = 2.37, P = .020), and left temporal lobe (F₁,₉₃ = 3.01, P = .003), with standardized effect sizes of -1.43, -1.3, and -1.0, respectively. CONCLUSIONS CACNA1C risk variant rs1006737 affects cortical white matter integrity in schizophrenia. Further imaging genetic investigations on the mediating effect of CACNA1C in schizophrenia can uncover brain circuitries involved in schizophrenia and suggest potential novel targets for intervention.
PLOS ONE | 2013
Jamie Yu Jin Thong; Anqi Qiu; Min Yi Sum; Carissa Nadia Kuswanto; Ta Ahn Tuan; Gary Donohoe; Yih Yian Sitoh; Kang Sim
Although the genome wide supported psychosis susceptibility neurogranin (NRGN) gene is expressed in human brains, it is unclear how it impacts brain morphology in schizophrenia. We investigated the influence of NRGN rs12807809 on cortical thickness, subcortical volumes and shapes in patients with schizophrenia. One hundred and fifty six subjects (91 patients with schizophrenia and 65 healthy controls) underwent structural MRI scans and their blood samples were genotyped. A brain mapping algorithm, large deformation diffeomorphic metric mapping, was used to perform group analysis of subcortical shapes and cortical thickness. Patients with risk TT genotype were associated with widespread cortical thinning involving frontal, parietal and temporal cortices compared with controls with TT genotype. No volumetric difference in subcortical structures (hippocampus, thalamus, amygdala, basal ganglia) was observed between risk TT genotype in patients and controls. However, patients with risk TT genotype were associated with thalamic shape abnormalities involving regions related to pulvinar and medial dorsal nuclei. Our results revealed the influence of the NRGN gene on thalamocortical morphology in schizophrenia involving widespread cortical thinning and thalamic shape abnormalities. These findings help to clarify underlying NRGN mediated pathophysiological mechanisms involving cortical-subcortical brain networks in schizophrenia.