Elevated postmortem monoamine oxidase B activity in the caudate nucleus in hUntington's disease compared to schizophrenics and controls

Mann, J. John; Kaplan, Richard D.; Bird, Edward D.

doi:10.1007/bf01249088

Cited by 42 publications

(14 citation statements)

References 19 publications

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“…(2) In Huntington's disease, no change in MAO-A activity but a significant increase in caudatus MAO-B activity was found in patients when compared with age-matched controls (Mann et al, 1986). Recently, Reynolds and Garrett …”

Section: Changes In Mao Activity and In Da And Homovanillic Acid (Hvamentioning

confidence: 97%

Dopamine-derived alkaloids in alcoholism and in Parkinson's and Huntington's diseases

Dostert¹,

Benedetti²,

Dordain

1988

J. Neural Transmission

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Tetrahydroisoquinoline (TIQ) alkaloids and 1-carboxy TIQ derivatives have been found in human fluids and/or tissues. The possible biosynthetic pathways of salsolinol (Sal), taken as an example of TIQs, are discussed, and the possibility that biosynthesis occurs through a stereospecific enzymatic reaction is considered. In this respect, it is reported that the R enantiomer of Sal predominates in urines of healthy volunteers, whereas the S enantiomer predominates in port wine and possibly in other beverages and foods, suggesting that Sal present in humans could have, at least partially, and endogenous enzymatic origin. TIQs and other dopamine-derived alkaloids are weak MAO inhibitors, the R enantiomer of Sal and salsolidine being more potent than the S form. The changes in monoamine oxidase activity and the nigrostriatal concentrations of dopamine and homovanillic acid in Parkinson's and Huntington's diseases and in alcoholism are reviewed. In these pathological situations, changes in the levels of dopamine-derived alkaloid levels may occur. The possibility that the modifications found might cause or contribute to changes in mental and/or neurophysiological states in these pathological situations is considered.

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Section: Changes In Mao Activity and In Da And Homovanillic Acid (Hvamentioning

confidence: 97%

Dopamine-derived alkaloids in alcoholism and in Parkinson's and Huntington's diseases

Dostert¹,

Benedetti²,

Dordain

1988

J. Neural Transmission

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“…It has been reported that the brain MAO-B activity is increased with aging (Fowler et al, 1980) and in certain neurodegenerative diseases such as Alzheimer's disease (Adolfsson et al, 1980;Jossan et al, 1991 a;Oreland and Gottfries, 1986), Parkinson's disease (Riederer and Jellinger, 1983;Schneider et al, 1981), and Huntington's chorea (Mann et al, 1980(Mann et al, , 1986Riederer and Jellinger, 1983). In Alzheimer and in ALS brain astrocytosis has been shown to occur (Duffy etal., 1980;Kushner etal., 1991).…”

Section: Introductionmentioning

confidence: 94%

Increased binding of3H-L-deprenyI in spinal cords from patients with amyotrophic lateral sclerosis as demonstrated by autoradiography

Aquilonius¹,

Jossan²,

Ekblom³

et al. 1992

J. Neural Transmission

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The present investigation has applied quantitative autoradiography and histochemistry to study the regional distribution of MAO-B and its relation to the number of cells in respective regions. L-deprenyl binds irreversibly and quantitatively to the B-form of monoamine oxidase, MAO, and is an ideal 3H-ligand to measure the MAO-B enzyme protein in tissues by means of in vitro autoradiography. The investigation is performed on spinal sections from five controls and five cases with amyotrophic lateral sclerosis (ALS) on cervical, thoracic and lumbar level. The highest density of 3H-L-deprenyl binding was found around the central canal (lamina X). MAO-B was markedly increased (up to 2.5 times of values in controls) specifically in regions of neurodegeneration e.g. motor neuron laminae and corticospinal tracts. There was a high correlation between glial cell count and 3H-L-deprenyl binding with a relation indicating enhanced MAO-B protein in glial cells within areas of neurodegeneration. In contrast the increased microglial cell number in ALS did not show any correlation with 3H-L-deprenyl binding.

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“…1 Given these roles it has been proposed that abnormalities of MAO-B level and function contribute to the pathology of Alzheimer's disease, Parkinson's disease, Huntington's disease, major depressive disorder, and substance abuse. 1 To date, investigations have largely focused on Alzheimer's disease, for which abnormally elevated MAO-B levels in the prefrontal cortex are frequently found, 4 and Huntington's disease, for which elevated MAO-B level in the striatum was reported, 5 and cigarette smoking, for which globally reduced MAO-B binding was found. 6 Selective MAO-B inhibitor therapeutics have been approved for the treatment of major depressive disorder and Parkinson's disease and are under development for Alzheimer's disease.…”

Section: Monoamine Oxidase B (Mao-b)mentioning

confidence: 99%

Kinetic Modeling of the Monoamine Oxidase B Radioligand [¹¹C]SL25.1188 in Human Brain with High-Resolution Positron Emission Tomography

Rusjan

Wilson

Miler

et al. 2014

J Cereb Blood Flow Metab

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This article describes the kinetic modeling of [ 11 C]SL25.1188 ([(S)-5-methoxymethyl-3-[6-(4,4,4-trifluorobutoxy)11 C]one]) binding to monoamine oxidase B (MAO-B) in the human brain using high-resolution positron emission tomography (PET). Seven healthy subjects underwent two separate 90-minute PET scans after an intravenous injection of [ 11 C]SL25.1188. Complementary arterial blood sampling was acquired. Radioactivity was quickly eliminated from plasma with 80% of parent compound remaining at 90 minutes. Metabolites were more polar than the parent compound. Time-activity curves showed high brain uptake, early peak and washout rate consistent with known regional MAO-B concentration. A two-tissue compartment model (2-TCM) provided better fits to the data than a 1-TCM. Measurement of total distribution volume (V T ) showed very good identifiability (based on coefficient of variation (COV)) for all regions of interest (ROIs) (COV(V T )o8%), low betweensubject variability (B20%), and quick temporal convergence (within 5% of final value at 45 minutes). Logan graphical method produces very good estimation of V T . Regional V T highly correlated with previous postmortem report of MAO-B level (r 2 ¼ X0.9). Specific binding would account from 70% to 90% of V T . Hence, V T measurement of [11 C]SL25.1 1 88 PET is an excellent estimation of MAO-B concentration.

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Elevated postmortem monoamine oxidase B activity in the caudate nucleus in hUntington's disease compared to schizophrenics and controls

Cited by 42 publications

References 19 publications

Dopamine-derived alkaloids in alcoholism and in Parkinson's and Huntington's diseases

Dopamine-derived alkaloids in alcoholism and in Parkinson's and Huntington's diseases

Increased binding of3H-L-deprenyI in spinal cords from patients with amyotrophic lateral sclerosis as demonstrated by autoradiography

Kinetic Modeling of the Monoamine Oxidase B Radioligand [¹¹C]SL25.1188 in Human Brain with High-Resolution Positron Emission Tomography

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Elevated postmortem monoamine oxidase B activity in the caudate nucleus in hUntington's disease compared to schizophrenics and controls

Cited by 42 publications

References 19 publications

Dopamine-derived alkaloids in alcoholism and in Parkinson's and Huntington's diseases

Dopamine-derived alkaloids in alcoholism and in Parkinson's and Huntington's diseases

Increased binding of3H-L-deprenyI in spinal cords from patients with amyotrophic lateral sclerosis as demonstrated by autoradiography

Kinetic Modeling of the Monoamine Oxidase B Radioligand [11C]SL25.1188 in Human Brain with High-Resolution Positron Emission Tomography

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Product

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Kinetic Modeling of the Monoamine Oxidase B Radioligand [¹¹C]SL25.1188 in Human Brain with High-Resolution Positron Emission Tomography