Paola Magioncalda

Assistant Professor

PSYCHIATRIC NEUROSCIENCE LAB                                                                                                                        Our lab investigates the relationship of brain functioning with phenomenal experience and behavior in physiology and psychopathology.


My academic training and research experience have provided me with a background in psychiatry and neuroscience. After graduating from medical school and specializing in psychiatry (University of Genoa, Italy), I obtained my PhD degree in neuroscience (University of Genoa, Italy) and a postgraduate research master degree in affective neuroscience (Maastricht University, Netherlands). During the last years, I conducted my research work at the Department of Neuroscience of the University of Genoa (Italy) as a research fellow. I also spent several periods of training and research work at various international research centers as visiting researcher, including the Mind Brain Imaging and Neuroethics center (University of Ottawa, Canada), Icahn School of Medicine at Mount Sinai (New York, U.S.), Research Center for Brain and Consciousness (Taipei Medical University, Taiwan), and Mental Health Centre and Psychiatric Laboratory (Sichuan University, Chengdu, China). Finally, I joined Taipei Medical University as a medical researcher.

My research mainly focuses on the neurobiology of major psychiatric disorders, bipolar disorder especially. I investigate the structural brain alterations in bipolar disorder, in particular microstructural white matter damages, and how these are related to immunological changes. Moreover, I study how such structural brain abnormalities are related to changes in the functional architecture of intrinsic brain activity and, in turn, how these may manifest in the manic and depressive symptomatology of bipolar disorder. Finally, I am interested in a dimensional approach to psychiatric disorders, in order to detect the fundamental alterations in psychopathology that cut across the different clinical categories. This may help in the detection of more specific neurobiological alterations in psychiatric disorders and, potentially, to the implementation of more efficacious therapies.

My research work is conducted in strict collaboration with Dr. Matteo Martino. We are currently working on these research lines and implementing a unified model of the pathophysiology of bipolar disorder, as well as a working model of the relationship between brain functioning and psychopathology.

1. Magioncalda P and Martino M. A unified model of the pathophysiology of bipolar disorder. Molecular Psychiatry. 2022

2. Martino M and Magioncalda P. Tracing the psychopathology of bipolar disorder to the functional architecture of intrinsic brain activity and its neurotransmitter modulation: a three-dimensional model. Molecular Psychiatry. 2022

Three-dimensional model of brain functioning and phenomenal-behavioral dimensions. Abbreviations: SMN, sensorimotor network; SN, salience network; aDMN, anterior default-mode network; pDMN, posterior default-mode network; CEN, central executive network; PACC, perigenual anterior cingulate cortex; SACC, supragenual anterior cingulate cortex; MCC, middle cingulate cortex; PCC, posterior cingulate cortex; C BG, central basal ganglia; V BG, ventral basal ganglia; D BG, dorsal basal ganglia; DM Thal, dorsomedial nucleus of thalamus; V Thal, ventral nuclei of thalamus; Pul Thal, pulvinar nucleus of thalamus; VTA, ventral tegmental area; SNc, substantia nigra; RNi, raphe nuclei.

Unified model of the pathophysiology of bipolar disorder. Damage in the limbic network and alteration of neurotransmitter signaling (lower part). According to the model, the core pathophysiological mechanism in BD could be traceable to an immune-mediated white matter alteration resulting in a limbic network damage, which destabilizes the neurotransmitter signaling increasing its susceptibility to perturbations. Functional reconfiguration of intrinsic brain activity and psychopathology (upper part). Changes in neurotransmitter signaling (triggered by heterogeneous stressors and inflammatory states onto a damaged limbic network) may then lead to phasic reconfigurations of intrinsic brain activity, from abnormal subcortical-cortical coupling to changes in network balancing. Finally, this may clinically manifest in the psychopathological alterations of mania and depression. Abbreviations: BD, bipolar disorder; OFC, orbitofrontal cortex; sgACC, subgenual anterior cingulate cortex; Amy, amygdala; HypoT, hypothalamus; Ant Thal, anterior nuclei of thalamus; HIPPO, hippocampus; NT n, neurotransmitter-related nuclei; DA, dopamine; 5HT, serotonin; SNc/VTA, substantia nigra/ventral tegmental area; RNi, raphe nuclei; BG, basal ganglia; Thal, thalamus; SN, salience network; SMN, sensorimotor network; DMN, default-mode network

For more information on my ongoing projects, please see here. For the complete list of my published work, please see My Bibliography