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A Ploska

Publications and source records attributed to A Ploska.

8 recordsLinked to original sources
PubMed1991

Severity and specificity of cognitive impairment in Alzheimer's, Huntington's, and Parkinson's diseases and progressive supranuclear palsy.

To investigate differences in severity and specificity of cognitive impairment among various neurodegenerative diseases, we tested groups of patients presenting with senile dementia of the Alzheimer type (SDAT; 44), progressive supranuclear palsy (PSP; 45), Huntington's disease (HD; 35) and Parkinson's disease (PD; 164), with an extensive neuropsychological battery. We found dementia, as defined by a global intellectual performance 2 standard deviations lower than mean control values, in 93% of SDAT, 66% of HD, 58% of PSP, and 18% of PD patients. Specific features of cognitive impairment distinguished the four groups of patients once they were matched for level of intellectual deterioration: remote memory and linguistic disorders in SDAT, frontal lobe-like abnormalities in PSP, concentration and acquisition disorders in HD. There was no specific alteration in demented PD patients. This study demonstrates the frequency of dementia in predominantly subcortical degenerative diseases and indicates that "subcortical dementia," rather than being a homogeneous entity, should be divided into specific subtypes of cognitive impairment related to different underlying specific lesions of each disease.

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PubMed1989

Continuous and intermittent levodopa differentially affect basal ganglia function.

The effects of continuous and intermittent levodopa treatment on behavioral and biochemical indexes of basal ganglia function were compared in rats with unilateral 6-hydroxydopamine lesions of the nigrostriatal dopamine pathway. Animals treated for 30 days with intermittent levodopa exhibited behavioral sensitization manifested by an enhanced rotational response to apomorphine; the rotational response of rats treated with an equivalent dose of levodopa by continuous infusion did not differ from that of saline-treated controls. Dopamine receptor up-regulation in the denervated striatum relative to the intact striatum was statistically significant for D1 but not D2 receptors: This asymmetry in dopamine receptor levels was diminished following intermittent levodopa treatment. Glutamic acid decarboxylase activity, modestly elevated in all groups in the denervated striatum relative to the intact striatum, increased substantially over control values bilaterally as a result of intermittent, but not continuous, levodopa treatment. These findings suggest a relation between the schedule of chronic levodopa administration and the development of behavioral sensitization, possibly as a consequence of alterations in neuronal systems located downstream from striatal dopamine receptors. The behavioral sensitization induced by chronic, intermittent dopaminomimetic treatment may serve as a model for motor fluctuations in Parkinson's disease.

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PubMed1988

[3H]dihydrotetrabenazine, a new in vitro monoaminergic probe for human brain.

The monoamine transporter of dopamine (DA), noradrenaline, and 5-hydroxytryptamine synaptic vesicles was assayed in rat and human brain homogenates by in vitro binding of [3H]dihydrotetrabenazine. [3H]Reserpine, a second ligand of the vesicular monoamine transporter, could not be used. [3H]Dihydrotetrabenazine binding in rat brain was stable after 72 h at 22 degrees C postmortem. In major human brain regions, [3H]dihydrotetrabenazine binding was specific and saturable (KD, 2.7 nM). Displacement constants by substrates or inhibitors of vesicular monoamine uptake, and regional distribution in human brain were similar to those found in rodents. The highest densities of binding sites were observed in caudate nucleus, putamen, and accumbens nucleus. In caudate nucleus and in putamen from normal human subjects, [3H]dihydrotetrabenazine binding and homovanillic acid concentration were significantly or nearly significantly correlated. A weaker correlation was found between [3H]dihydrotetrabenazine binding and DA, in association with a higher variability of DA. [3H]Dihydrotetrabenazine binding in caudate nucleus and in putamen decreased significantly with age, unlike DA and homovanillic acid concentrations. The results establish [3H]dihydrotetrabenazine as a presynaptic monoaminergic ligand of interest for studies on postmortem human brain.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1987

Dopamine D-1 receptor and cyclic AMP-dependent phosphorylation in Parkinson's disease.

D-1 and D-2 receptor densities, evaluated respectively by [3H]SCH 23390 and [3H]spiperone binding, and DARPP-32 (dopamine and adenosine 3':5'-monophosphate-regulated phosphoprotein-32K) concentrations, were studied in the brains of control and parkinsonian subjects postmortem. D-2 receptor density was unchanged in the putamen of parkinsonian patients. D-1 receptor density was unchanged in the putamen and substantia nigra pars reticulata (SNR) of parkinsonian patients, but decreased by 28% in the substantia nigra pars compacta (SNC). DARPP-32, which is localized in the same structures as D-1 receptors of which it is thought to represent the intracellular messenger, decreased by 45% in the putamen, 66% in the SNR, and 79% in the SNC. The decrease in D-1 receptors in the SNC may be due to degeneration of pallidonigral GABAergic neurons, but some of the D-1 receptors may be on the nigrostriatal dopaminergic neurons themselves. The dissociation between the alteration of D-1 receptor densities and DARPP-32 concentrations in both the striatum and substantia nigra, which are of the same order in the two structures, may be an index of functional hypoactivity of D-1 neurotransmission.

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PubMed1986

Cellular localization of adrenergic receptors in rat and human brain.

The localization of adrenergic receptors in the central nervous system was studied in two physiological conditions of noradrenergic denervation, a 6-hydroxydopamine-induced lesion of the locus coeruleus in newborn rat, and a pathological related degeneration of the locus coeruleus in man, Parkinson's disease. The localization of these receptors in the synapse has been studied with the technique of subcellular fractionation by differential centrifugation. In lesioned rats, an increase in the density of alpha 1 and beta 1 receptors was observed in several brain regions, in contrast to alpha 2 receptors which were not modified. Subcellular fractionation in lesioned rats showed an increase in alpha 1 and beta 1 receptors in synaptosomal fractions. Similar results were found in parkinsonian patients: alpha 1 receptors increased in the synaptosomal fraction; beta receptors increased in synaptosomal and microsomal fractions. These results suggest that alpha 1 and beta 1 receptors may be located on non-noradrenergic nerve terminals in mammalian brain. alpha 2 and beta 2 receptors may be situated on glial cells or neuronal elements unrelated to noradrenergic input.

Animals↗
PubMed1985

High and low affinity [3H]imipramine binding sites in control and parkinsonian brains.

[3H]Imipramine binding was studied in the prefrontal cortex and putamen of post-mortem brains from control and Parkinsonian subjects. Saturation and inhibition curves showed both high affinity [3H]imipramine binding related to the serotonin uptake mechanism and low affinity binding which was sodium-independent and unrelated to serotonergic uptake. After subcellular fractionation, high affinity [3H]imipramine binding sites were enriched in synaptosomal fractions. In Parkinson's disease, where brain serotonin concentrations are decreased, there was a significant reduction in the density of the high affinity binding in the prefrontal cortex and putamen while the characteristics of the low affinity binding sites remained unchanged. After subcellular fractionation of the putamen of Parkinsonian patients, the decrease in [3H]imipramine binding was found predominantly in the synaptosomal fractions. These results are consistent with a relation between the high affinity [3H]imipramine binding sites and the neuronal serotonin uptake mechanism. Estimation of [3H]imipramine binding could be used as a specific marker for the study of serotonergic innervation in human post-mortem material. The reduction in the density of tricyclic antidepressant binding sites found in cortical and subcortical areas of Parkinsonian brains may be somehow implicated in the depression often seen in patients.

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