Author
Peter Bjurling
Bio: Peter Bjurling is an academic researcher from Uppsala University. The author has contributed to research in topics: Positron emission tomography & Dopaminergic. The author has an hindex of 25, co-authored 55 publications receiving 2157 citations.
Papers
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TL;DR: Suicide enzyme inactivators labeled with positron emitters can be used to quantitate the distribution and kinetic characteristics of MAO in human brain structures and show rapid clearance of the inactive enantiomer and retention of the active enantiomers within MAO B-rich brain structures.
Abstract: The regional distributions of monoamine oxidase (MAO) types A and B have been identified in human brain in vivo with intravenously injected 11C-labeled suicide enzyme inactivators, clorgyline and L-deprenyl, and positron emission tomography. The rapid brain uptake and retention of radioactivity for both 11C tracers indicated irreversible trapping. The anatomical distribution of 11C paralleled the distribution of MAO A and MAO B in human brain in autopsy material. The corpus striatum, thalamus, and brainstem contained high MAO activity. The magnitudes of uptake of both [11C]clorgyline and L-[11C]deprenyl were markedly reduced in one subject treated with the antidepressant MAO inhibitor phenelzine. A comparison of the brain uptake and retention of the 11C-labeled inactive (D-) and active (L-) enantiomers of deprenyl showed rapid clearance of the inactive enantiomer and retention of the active enantiomer within MAO B-rich brain structures, in agreement with the known stereoselectivity of MAO B for L-deprenyl. Prior treatment with unlabeled L-deprenyl prevented retention of L-[11C]deprenyl. Thus, suicide enzyme inactivators labeled with positron emitters can be used to quantitate the distribution and kinetic characteristics of MAO in human brain structures.
372 citations
TL;DR: In vivo by PET neurochemical effects induced in brain by treatment with tacrine to Alzheimer patients show increased binding of (S)(-)11C-nicotine in brain compatible with a restoration of nicotinic cholinergic receptors.
144 citations
TL;DR: PET with carbon-11-labeled 5-HTP demonstrated high uptake in neuroendocrine gastrointestinal tumors and thereby allowed improved visualization compared with CT, indicating the potential of 11C-5- HTP-PET as a means to monitor therapy.
Abstract: PURPOSECarcinoid tumors, especially those of midgut origin, produce serotonin via the precursors tryptophan and 5-hydroxytryptophan (5-HTP). We have evaluated the usefulness of positron emission tomography (PET) with carbon-11-labeled 5-HTP in the diagnosis and treatment follow-up evaluation of patients with neuroendocrine tumors.PATIENTS AND METHODSPET using 11C-labeled 5-HTP was compared with computed tomography (CT) in 18 patients (14 midgut, one foregut, one hindgut carcinoid, and two endocrine pancreatic tumors [EPT]). In addition, 10 of 18 patients were monitored with PET examinations during treatment.RESULTSAll 18 patients, including two with normal urinary 5-hydroxyindole acetic acid (U-5-HIAA), had increased uptake of 11C-labeled 5-HTP in tumorous tissue as compared with normal tissue. Liver metastases, as well as lymph node, pleural, and skeletal metastases, showed enhanced 5-HTP uptake and PET could detect more lesions than CT in 10 patients and equal numbers in the others. Tumor visibility was...
140 citations
TL;DR: MRI revealed that the manganese accumulated in the globus pallidus, putamen and caudate nucleus and there were also suggestions of gliosis/edema in the posterior limb of the internal capsule, which supports the suggestion that dopaminergic nerve endings degenerate duringManganese intoxication.
Abstract: A series of positron emission tomography scans was made on two monkeys during a 16-month period when they received manganese(IV)oxide by subcutaneous injection. The distribution of [11C]-nomifensine uptake, indicating dopamine terminals, was followed in both monkey brains. The brain distributions of [11C]-raclopride, demonstrating D2 dopamine receptors, and [11C]-l-dopa, as a marker of dopamine turnover, were followed in one monkey each. The monkeys developed signs of poisoning namely unsteady gait and hypoactivity. The [11C]-nomifensine uptake in the striatum was reduced with time and reached a 60% reduction after 16 months exposure. This supports the suggestion that dopaminergic nerve endings degenerate during manganese intoxication. The [11C]-l-dopa decarboxylation was not significantly altered indicating a sparing of [11C]-l-dopa decarboxylation during manganese poisoning. A transient decrease of [11C]-raclopride binding occurred but at the end of the study D2-receptor binding had returned to starting values. The magnetic resonance imaging (MRI) revealed that the manganese accumulated in the globus pallidus, putamen and caudate nucleus. There were also suggestions of gliosis/edema in the posterior limb of the internal capsule. MRI might be useful to follow manganese intoxication in humans as long as the scan is made within a few months of exposure to manganese, i. e. before a reversal of the manganese accumulation.
125 citations
TL;DR: It is shown that specific binding of [11C]nomifensine in the lesioned striatum disappears to a large extent as a result of the lesion, indicating a corresponding loss of striatal dopamine re-uptake binding sites and thus of the dopamine nerve terminal pool.
106 citations
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TL;DR: A system has been described that links the medial prefrontal cortex and a few related cortical areas to the amygdala, the ventral striatum and pallidum, the medial thalamus, the hypothalamus, and the periaqueductal gray and other parts of the brainstem, which indicates that this system is centrally involved in mood disorders.
1,386 citations
TL;DR: Findings implicate interconnected neural circuits in which pathologic patterns of neurotransmission may result in the emotional, motivational, cognitive, and behavioral manifestations of primary and secondary affective disorders.
1,280 citations
TL;DR: This work evaluates claims and some counter-claims made about the physiological importance of these enzymes and the potential of their inhibitors in the light of what the authors know, and still have to learn, of the structure, function and genetics of the monoamine oxidases and the disparate actions of their inhibitor.
Abstract: Monoamine oxidase inhibitors were among the first antidepressants to be discovered and have long been used as such. It now seems that many of these agents might have therapeutic value in several common neurodegenerative conditions, independently of their inhibition of monoamine oxidase activity. However, many claims and some counter-claims have been made about the physiological importance of these enzymes and the potential of their inhibitors. We evaluate these arguments in the light of what we know, and still have to learn, of the structure, function and genetics of the monoamine oxidases and the disparate actions of their inhibitors.
1,173 citations
TL;DR: A neuropsychological theory is proposed that assumes category learning is a competition between separate verbal and implicit categorization systems and that the anterior cingulate and prefrontal cortices are critical to the verbal system.
Abstract: A neuropsychological theory is proposed that assumes category learning is a competition between separate verbal and implicit (i.e., procedural-learning-based) categorization systems. The theory assumes that the caudate nucleus is an important component of the implicit system and that the anterior cingulate and prefrontal cortices are critical to the verbal system. In addition to making predictions for normal human adults, the theory makes specific predictions for children, elderly people, and patients suffering from Parkinson's disease, Huntington's disease, major depression, amnesia, or lesions of the prefrontal cortex. Two separate formal descriptions of the theory are also provided. One describes trial-by-trial learning, and the other describes global dynamics. The theory is tested on published neuropsychological data and on category learning data with normal adults.
1,114 citations
Journal Article•
TL;DR: The enzyme responsible for the O- methylation, catechol- O -methyltransferase (COMT) was partly purified and characterized by the same group as EC, which first described the enzyme-catalyzed O-methylation of catechlamines and other catechols in the late 1950s.
Abstract: [Axelrod et al. (1958)][1] first described the enzyme-catalyzed O- methylation of catecholamines and other catechols in the late 1950s. The enzyme responsible for the O- methylation, catechol- O -methyltransferase (COMT; EC[2.1.1.6][2]),2 was partly purified and characterized by the same group ([
1,078 citations