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@PHDTHESIS{Chen:884904,
author = {Chen, Ji},
title = {{M}odeling the psychopathology in schizophrenia: symptom
dimensions, subtypes, brain connectivity patterns, and
molecular architecture},
school = {Heinrich-Heine Universität},
type = {Dissertation},
reportid = {FZJ-2020-03308},
pages = {147},
year = {2020},
note = {Dissertation, Heinrich-Heine Universität, 2020},
abstract = {Summary Schizophrenia is a severe, debilitating, and
heterogeneous mental disorder. Disentangling the
psychopathological heterogeneity in schizophrenia from its
underlying dimensions and the related neurobiology remains a
challenge. Although ample efforts have been devoted to their
study, symptom dimensions and subtypes, as well as
neurobiological substrates and differentiations in
schizophrenia remain unclear. In my project, I implemented
machine-learning frameworks aiming to develop a new method
to robustly and reliably conceptualize the psychopathology
of schizophrenia at both symptom and brain levels in a
data-driven fashion. First, an orthonormal and projective
variant of non-negative matrix factorization (OPNMF) was
employed to identify the latent dimensions of the
well-established Positive and Negative Syndrome Scale
(PANSS). This method is capable of learning compact and
homogeneous factors which can be readily generalized to
novel patients. By evaluating OPNMF-derived factor models
within a large, homogeneous schizophrenia dataset and then
cross-validating the yielded models with an independent
multi-site sample recruited from Europe, Asia, and the
United States, a structure with four dimensions representing
negative, positive, affective and cognitive symptoms was
identified as the most stable and generalizable. This
four-dimensional structure showed higher internal
consistency than the original PANSS subscales and previously
proposed factor models. Based on the identified dimensions,
fuzzy-clustering was employed to derive symptomatically
well-separated schizophrenia subtypes. Two core subtypes of
schizophrenia patients were identified, with one featuring
prominent negative and affective symptoms while the other
featuring positive symptomatology. This positive-negative
dichotomy was longitudinally stable in about $80\%$ of the
repeatedly assessed patients. Neurobiological divergence of
the identified subtypes was assessed using classification
analysis of resting-state functional MRI measurement with
cross-validation in a subset of the multi-site sample.
Individual subtypes could be well-discriminated using
resting-state functional connectivity (rsFC) profiles of the
ventromedial frontal cortex, temporoparietal junction, and
precuneus, with the highest classification accuracy of
$70\%.$ Individual expression of the four symptom dimensions
were predicted using relevance vector machine based on rsFC
within 17 meta-analytically defined task-activation
networks. A strict validation procedure including 10-fold
cross-validation, leave-one-site-out experiments, and
generalization to independent samples was conducted to
derive robust symptom-network associations. Finally, the
significant and robust symptom-predictive networks were
spatially correlated with whole-brain density maps of nine
receptors and transporters from prior molecular imaging in
healthy populations to reveal the molecular architecture
related to these networks. The theory-of-mind and the
extended socio-affective default networks, which are
implicated in social cognition and affective processes, were
identified as significantly and robustly predictive of the
cognitive symptom dimension. Moreover, node importance of
these two networks showed a spatial pattern positively
co-varying with D1 dopamine receptor and serotonin reuptake
transporter densities as well as presynaptic dopamine
capacity.The current work provides a systematic modeling
framework of schizophrenia from symptomatology to
neurobiology. Together the proposed hybrid
dimensional-categorical conceptualization of symptomatology
and the revealed intrinsic neurobiological processes and
molecular architecture further disentangle the heterogeneity
in schizophrenia, possibly allowing for the development of
more specifically targeted treatments.},
cin = {INM-7},
cid = {I:(DE-Juel1)INM-7-20090406},
pnm = {574 - Theory, modelling and simulation (POF3-574)},
pid = {G:(DE-HGF)POF3-574},
typ = {PUB:(DE-HGF)11},
url = {https://juser.fz-juelich.de/record/884904},
}