Our findings indicate a tight coupling between processes disrupting performance and neural network adaptation, the patterns of which appear to be both task- and individually-unique. We propose that connectivity fingerprinting offers potential as a clinical marker to track adaptation of specific functional networks across treatment interventions over time. Although the thalamus is a key structure in the pathophysiology of obsessive-compulsive disorder (OCD), reports regarding thalamic volume alterations in OCD patients have been inconsistent. Because the thalamus has a complex structure with distinct functions, we investigated subregional volume changes in the thalamus and their relationship with clinical attributes in a large sample of medication-free OCD patients. We collected T1-weighted magnetic resonance imaging data from 177 OCD patients and 152 healthy controls (HCs). Using FreeSurfer, we segmented the thalamus into 12 nuclei groups; subregional volumes were compared between groups using an analysis of covariance. The relationships between altered thalamic volumes and OC symptom severity and OCD onset age were investigated. Compared to HCs, OCD patients showed a smaller volume of the left posterior thalamic nuclei. Other thalamic subregions did not show significant group differences. There was a significant negative correlation between the volume of the left posterior thalamic nuclei and the age of OCD onset but no significant correlation with OC symptom severity. This is the first study to report reduced volume of the posterior thalamic nuclei in a large sample of medication-free OCD patients. Our results suggest that the volume of posterior thalamic nuclei may reflect different pathophysiological mechanisms of OCD subtypes related to the age of onset. Additional studies with pediatric samples are required to clarify the relationship between thalamic alterations and the onset age of OCD.This is the first study to report reduced volume of the posterior thalamic nuclei in a large sample of medication-free OCD patients. Our results suggest that the volume of posterior thalamic nuclei may reflect different pathophysiological mechanisms of OCD subtypes related to the age of onset. Additional studies with pediatric samples are required to clarify the relationship between thalamic alterations and the onset age of OCD. Neuropsychological test-specific neural substrates in subcortical vascular cognitive impairment (SVCI) are expected to differ from those in Alzheimer's disease-related cognitive impairment (ADCI) but the details are unclear. To determine neural substrates related to cerebral small vessel disease, we investigated the correlations between cognitive dysfunctions measured by standardized neuropsychological tests and cortical thickness in a large sample of participants with amyloid negative (Aβ (-)) SVCI. One hundred ninety-eight participants with Aβ (-) SVCI were recruited from the memory clinic between November 2007 to August 2018. To acquire neural substrates, we performed linear regression using the scores of each neuropsychological test as a predictor, cortical thickness as an outcome, and age, sex, education years, intracranial volume and white matter hyperintensity (WMH) as confounders. Poor performances in each neuropsychological test were associated with cortical atrophy in certain brain regions regardless of WMH. Especially, not the medial temporal but the frontal and posterior cingulate regions with cortical atrophy were mainly associated with memory impairment. Poor performance in animal fluency was more likely to be associated with cortical atrophy in the left hemisphere, while poor performance in the visuospatial memory test was more likely to be associated with cortical atrophy in the right hemisphere. Our findings suggested that cortical atrophy was an important factor of cognitive impairment in Aβ (-) SVCI regardless of WMH. Furthermore, our findings might give clinicians a better understanding of specific neural substrates of neuropsychological deficits in patients with SVCI.Our findings suggested that cortical atrophy was an important factor of cognitive impairment in Aβ (-) SVCI regardless of WMH. Furthermore, our findings might give clinicians a better understanding of specific neural substrates of neuropsychological deficits in patients with SVCI. Moyamoya vasculopathy is a rare, often bilateral disease characterized by progressive stenosis and occlusion of the distal internal carotid artery, leading to a progressive deterioration of cerebrovascular reactivity (CVR) and increased risk of transient ischemic attacks (TIAs), infarction and hemorrhage. Surgical revascularization is a widely accepted symptomatic treatment, often performed bilaterally in one or two stages. To possibly further optimize treatment strategy, we investigated the effect of unilateral revascularization surgery on the CVR of, and TIA frequency originating from, the contralateral hemisphere. From our database of 143 moyamoya vasculopathy patients we selected those with bilateral disease, who underwent hemodynamic imaging ([15O]H2O positron emission tomography (PET)-CT with acetazolamide challenge) before and 14months (median) after unilateral revascularization. We evaluated CVR in three regions per hemisphere, and averaged these per hemisphere for statistical comparison. Conservacan improve after unilateral revascularization surgery in bilateral MMV.Both CVR and TIA frequency in the contralateral hemisphere can improve after unilateral revascularization surgery in bilateral MMV.An interplay of early environmental and genetic risk factors with recent stressful life events (SLEs) in adulthood increases the risk for adverse mental health outcomes. The interaction of early risk and current SLEs on brain structure has hardly been investigated. Whole brain voxel-based morphometry analysis was performed in N = 786 (64.6% female, mean age = 33.39) healthy subjects to identify correlations of brain clusters with commonplace recent SLEs. learn more Genetic and early environmental risk factors, operationalized as those for severe psychopathology (i.e., polygenic scores for neuroticism, childhood maltreatment, urban upbringing and paternal age) were assessed as modulators of the impact of SLEs on the brain. SLEs were negatively correlated with grey matter volume in the left medial orbitofrontal cortex (mOFC, FWE p = 0.003). This association was present for both, positive and negative, life events. Cognitive-emotional variables, i.e., neuroticism, perceived stress, trait anxiety, intelligence, and current depressive symptoms did not account for the SLE-mOFC association.