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Harry Vilkman

Researcher at University of Turku

Publications -  24
Citations -  2158

Harry Vilkman is an academic researcher from University of Turku. The author has contributed to research in topics: Dopamine receptor D2 & Dopamine. The author has an hindex of 19, co-authored 24 publications receiving 2084 citations.

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Age-related dopamine D2/D3 receptor loss in extrastriatal regions of the human brain.

TL;DR: The results indicate that the previously demonstrated age-related decline in striatal dopamine D2 receptors extends to several extrastriatal regions in normal human males, and the rate of D2/3R decline may be faster in the frontal cortex as compared to the temporal and thalamic regions.
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Depressive symptoms and presynaptic dopamine function in neuroleptic-naive schizophrenia

TL;DR: The major finding in this study is that depressive symptoms in neuroleptic-naive first-admission schizophrenia are associated with low presynaptic dopamine function, which appears to be hemisphere-related and may have drug-treatment implications, e.g., in prediction of response to D2 receptor blocking antipsychotic drugs.
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Sex differences in striatal presynaptic dopamine synthesis capacity in healthy subjects

TL;DR: Women had significantly higher striatal [(18)F]fluorodopa uptake (Ki values) than men and this finding may be associated with sex differences in vulnerability and clinical course of neuropsychiatric disorders with dopaminergic dysregulation, e.g., schizophrenia, alcohol dependence, and Parkinson's disease.
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High levels of dopamine activity in the basal ganglia of cigarette smokers

TL;DR: Smoking is related to greater dopamine activity in the human basal ganglia and nicotine-induced dopamine activity may be a relevant mechanism in dependence on cigarette smoking.
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Striatal Dopamine Transporter Binding in Neuroleptic-Naive Patients With Schizophrenia Studied With Positron Emission Tomography

TL;DR: Average striatal dopamine transporter density is unaltered in neuroleptic-naive patients with schizophrenia, however, patients lack asymmetry in caudate dopamine transporter binding, which conforms with disrupted brain lateralization in this disorder.