Jari Tiihonen

This study identifies a schizophrenia-associated radial glia cell state that disrupts early human brain development through single-cell transcriptomic and epigenomic analyses of organoids.

This study investigates dopamine D2R and opioid MOR receptor availabilities in ASD using PET imaging and finds reduced D2R availability in striatum and nucleus accumbens, and MOR changes in hippocampi and precuneus.

The paper shows human astrocytes influence neuronal network burst frequency via NMDA receptors, with differences between human and rat astrocytes and effects in schizophrenia-related cells.

This study shows that kynurenic acid promotes microglia-mediated synaptic pruning in schizophrenia by reducing neuronal activity and linking genetic risk variants to KYNA production.

This study finds reduced D2R availability in psychopathic offenders compared to controls, suggesting a potential neuromolecular pathway for psychopathy.

This study identifies eight genes associated with adult cognitive function through rare coding variants and shows how KDM5B dosage affects cognitive traits in mice and humans.

The paper investigates six rare SLCO1B1 variants in Finnish individuals with psychosis, finding one variant causes loss-of-function and reduced OATP1B1 protein expression.

This study investigates how mu-opioid receptor availability relates to brain responses to laughter and crying sounds in humans using PET-fMRI.

The paper constructs a CYP2D6 copy-number imputation panel and reports pharmacogenetic variant frequencies in Finnish individuals with psychosis, showing high imputation accuracy but limited clinical utility.

The paper compares neural responses to emotional stimuli in psychopathy and high-functioning autism, finding distinct patterns of somatomotor alterations.

The paper identifies molecular pathways and potential treatments for schizophrenia using stem cell-derived neurons and pharmacological associations.

The paper shows that astrocytes from schizophrenia patients exhibit transcriptional and functional changes, including inflammation and synaptic pathway alterations, which are partially reversible with clozapine treatment.