Schizophrenia is one of the most debilitating psychiatric disorders, characterized by heterogeneous clinical manifestations with positive symptoms, negative symptoms, cognitive deficits and affective symptoms. Due to the often-chronic relapsing disease courses and only limited treatment options, Schizophrenia is one of the top 15 global causes of disability and diminished quality of life associated with high socioeconomic costs for society and health care systems. Progress in developing a more effective individualized treatment and translate neurobiological findings into clinical practice has been hampered by the complex and multifactorial etiology involving multiple environmental, genetic and biological factors. In this context, the integration of advanced neuroimaging techniques with state-of-the art psychometric measures of symptoms and behaviour provides the opportunity to uncover the underlying pathological processes and to identify neuroimaging-derived biomarkers of distinct symptom domains. The six articles selected for this cumulative habilitation thesis illustrate how this integrative methodological approach can be applied in a dimensional and transdiagnostic research framework to examine neural substrates of symptom dimensions specifically focusing on reward system dysfunction and apathy. Using taskrelated fMRI, (1) we identified striatal hypoactivation during reward anticipation as specific neural marker of apathy in patients with schizophrenia, (2) examined different aspects of striatal subregion in the pathophysiology of apathy and (3) observed the association of blunted extra-striatal prefrontal activation with apathy induced reduced motor activity. (4) We found a potential dimensional mechanism of striatal dysfunction during reward processing ranging from nonclinical psychotic experiences in the general population to severe psychotic symptoms in early schizophrenia, (5) compared clinical and neural findings between schizophrenia and bipolar disorder to elucidate transdiagnostic neurobiological mechanisms of apathy and (6) applied DTI to examine the sensitivity of a novel fiber density measure in detecting symptom-specific microstructural white matter alterations of connections within the reward network. The presented results extend our understanding of impaired fronto-striatal reward system function in schizophrenia and demonstrate the successful application of neuroimaging methods to identify symptom-specific neural mechanisms. Taken together, this research approach could help develop neuroimaging-derived biomarkers for optimizing and individualizing treatment to improve clinical outcomes and reduce the high burden associated with this severe psychiatric disorder.